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1.
Dev Psychopathol. 2018 Aug;30(3):941-952. doi: 10.1017/S0954579418000664.

Prenatal CRH: An integrating signal of fetal distress.

Author information

1
University of California,Irvine.

Abstract

Corticotropin-releasing hormone (CRH) is distributed throughout the brain and in peripheral sites but primarily is localized in the paraventricular nucleus of the hypothalamus. It is a "master" stress hormone that is responsible for the synthesis of proopiomelanocortin (POMC) in the anterior pituitary gland. Behaviorally active peptide hormones, including adrenocorticotropin hormone (ACTH) and B-endorphin, are liberated from POMC by enzymes to activate critical processes during stress. CRH is not detectable in the circulation even during extreme stress. However, during human pregnancy, the human placenta expresses the gene for CRH (pCRH) resulting in detectable levels in maternal plasma that increases 20- to 40-fold over the course of gestation. Placental CRH is identical to CRH of hypothalamic origin in size, structure, immunoreactivity, and bioactivity. However, unlike the negative feedback between adrenal cortisol and hypothalamic CRH, cortisol stimulates the synthesis and release of pCRH. The bidirectional release of pCRH into maternal and fetal compartments is associated with regulating the timing of delivery, remodeling the fetal nervous system, and influencing developmental trajectories. Fetal exposure to pCRH during early and late gestation is associated with unique patterns of cortical thinning in school-age children. Placental CRH is elevated in response to physical and behavioral stress and may be an integrative marker of early adversity.

PMID:
30068427
DOI:
10.1017/S0954579418000664
[Indexed for MEDLINE]
Icon for Cambridge University Press
2.
Medicine (Baltimore). 2018 Jul;97(30):e11583. doi: 10.1097/MD.0000000000011583.

Ganglioglioma of the adenohypophysis mimicking pituitary adenoma: A case report and review of the literature.

Author information

1
Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine.
2
Brain Research Institute.
3
Collaborative Innovation Center for Brain Science, Zhejiang University, Hangzhou, Zhejiang, P.R. China.

Abstract

INTRODUCTION:

Ganglioglioma is a generally benign tumor, mostly occurring in patients <30 years old. Temporal lobe is most frequently involved. Up to now, only 3 cases were reported of ganglioglioma in the pituitary gland, all being confined to the neurohypophysis. Here, we are the first to report an adenohypophysis ganglioglioma.

CASE PRESENTATION:

A 43-year-old woman presented with chronic headache was referred to our hospital. Magnetic resonance imaging (MRI) indicated pituitary adenoma. Endoscopic transnasal transsphenoidal surgery was performed. The tumor was rich in blood supply, with tough texture, therefore only subtotal resection was conducted. Pathology analysis revealed an adenohypophysial tumor composed of dysplastic ganglion cells and neoplastic glial cells collided with nonspecific hyperplasia of pituitary cells. Immunohistochemistry revealed positive staining of synaptophysin, glial-fibrillary acidic protein, and CD34. The results were consistent with the diagnosis of ganglioglioma. After the surgery the patient recovered well except developing cerebrospinal fluid rhinorrhea, which was controlled by lumbar drainage. MRI 6 months later did not show any sign of progression.

CONCLUSION:

According to the findings of our case, concerns should be raised considering ganglioglioma as a differential diagnosis of mass located in the sellar region. Furthermore, an ideal management strategy for pituitary ganglioglioma is not known; therefore, more cases and long-term follow-up are needed to enrich our knowledge of the diagnosis, treatment, and prognosis of this rare intracranial lesion.

PMID:
30045287
PMCID:
PMC6078729
DOI:
10.1097/MD.0000000000011583
[Indexed for MEDLINE]
Free PMC Article
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3.
Horm Metab Res. 2018 Aug;50(8):640-647. doi: 10.1055/a-0633-2706. Epub 2018 Jul 18.

Expression of Peroxisome Proliferator-Activated Receptor Alpha (PPARα) in Non-Somatotroph Pituitary Tumours and the Effects of PPARα Agonists on MMQ Cells.

Author information

1
Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
2
Neuromed Institute, IRCCS, Pozzilli, Italy.
3
Endocrinology, CHU of Liège, University of Liège, Liège, Belgium.
4
Division of Pathology, "San Salvatore" Hospital, L'Aquila, Italy.
5
Department of Radiological, Oncological and Anatomopathological Sciences, University "La Sapienza", Rome, Italy.
6
Department of Neurology and Psychiatry, University "La Sapienza", Rome, Italy.

Abstract

Peroxisome proliferator-activated receptor alpha (PPARα) has been involved in the regulation of somatotroph tumour cells and may be targeted by different drugs, some of them are in current clinical use. The aim of this study was to investigate the expression of PPARα in additional phenotypes of pituitary adenomas (PA), the relationship between PPARα and its potential molecular partner aryl hydrocarbon receptor interacting protein (AIP) in these tumours, and the effects of PPARα agonists on lactotroph cells. Seventy-five human PA - 57 non-functioning (NFPA) and 18 prolactinomas (PRL-PA) - were characterised for PPARα and AIP expression by real time RT-PCR and/or immunohistochemistry (IHC), and the effects of fenofibrate and WY 14 643 on MMQ cells were studied in vitro. PPARα was expressed in a majority of PA. PPARα immunostaining was observed in 93.7% PRL-PA vs. 60.6% NFPA (p=0.016), the opposite being found for AIP (83.3% in NFPA vs. 43.7% in PRL-PA, p=0.003). PPARα expression was unrelated to gonadotroph differentiation in NFPA, but positively correlated with tumour volume in PRL-PA. Both drugs significantly reduced MMQ cell growth at high concentrations (100-200 μM). At the same time, despite modest stimulating effects on PRL secretion were observed, these were overcome by the reduction in cell number. In conclusion, PPARα is commonly expressed by PRL-PA and NFPA, regardless of AIP, and may represent a new target of PPARα agonists.

PMID:
30021235
DOI:
10.1055/a-0633-2706
[Indexed for MEDLINE]
Icon for Georg Thieme Verlag Stuttgart, New York
4.
Reprod Toxicol. 2018 Aug;79:72-78. doi: 10.1016/j.reprotox.2018.06.003. Epub 2018 Jun 12.

The anterior pituitary gap junctions: potential targets for toxicants.

Author information

1
Département de pathologie et biologie cellulaire, Faculté de Médecine, Université de Montréal, Montréal, QC Canada. Electronic address: maria.leiza.vitale@umontreal.ca.
2
Département de pathologie et biologie cellulaire, Faculté de Médecine, Université de Montréal, Montréal, QC Canada.

Abstract

The anterior pituitary regulates endocrine organs and physiological activities in the body. Environmental pollutants and drugs deleterious to the endocrine system may affect anterior pituitary activity through direct action on anterior pituitary cells. Within the gland, endocrine and folliculostellate cells are organized into and function as individual tridimensional networks, each network regulating its activity by coordinating the connected cells' responses to physiological or pathological cues. The gap junctions connecting endocrine cells and/or folliculostellate cells allow transmission of information among cells that is necessary for adequate network function. Toxicants may affect gap junctions as well as the physiology of the anterior pituitary. However, whether toxicants effects on anterior pituitary hormone secretion involve gap junctions is unknown. The folliculostellate cell gap junctions are sensitive to hormones, cytokines and growth factors. These cells may be an interesting experimental model for evaluating whether toxicants target anterior pituitary gap junctions.

KEYWORDS:

Anterior pituitary; Cell junctions; Folliculostellate cells; Gap junctions; Hormones toxicants

PMID:
29906538
DOI:
10.1016/j.reprotox.2018.06.003
[Indexed for MEDLINE]
Icon for Elsevier Science
5.
Toxicol Lett. 2018 Oct 1;295:41-53. doi: 10.1016/j.toxlet.2018.05.041. Epub 2018 Jun 2.

Protective mechanisms involving enhanced mitochondrial functions and mitophagy against T-2 toxin-induced toxicities in GH3 cells.

Author information

1
Department of Animal Sciences & Technology, Key Laboratory for the Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei, 430070, China.
2
Department of Animal Sciences & Technology, Laboratory of Quality & Safety Risk Assessment for Livestock and Poultry Products, Huazhong Agricultural University, Wuhan, Hubei, 430070, China.
3
Department of Animal Sciences & Technology, Key Laboratory for the Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei, 430070, China; Department of Animal Sciences & Technology, Laboratory of Quality & Safety Risk Assessment for Livestock and Poultry Products, Huazhong Agricultural University, Wuhan, Hubei, 430070, China. Electronic address: Wangxu@mail.hzau.edu.cn.
4
Department of Animal Sciences & Technology, Key Laboratory for the Detection of Veterinary Drug Residues, Huazhong Agricultural University, Wuhan, Hubei, 430070, China; Department of Animal Sciences & Technology, Laboratory of Quality & Safety Risk Assessment for Livestock and Poultry Products, Huazhong Agricultural University, Wuhan, Hubei, 430070, China. Electronic address: yuan5802@mail.hzau.edu.cn.

Abstract

T-2 toxin is the most toxic member of trichothecene mycotoxin. So far, the mechanism of mitochondrial toxicity and protective mechanism in mammalian cells against T-2 toxin are not fully understood. In this study, we aimed to investigate the cellular and mitochondrial toxicity of T-2 toxin, and the cellular protective mechanisms in rat pituitary GH3 cells. We showed that T-2 toxin significantly increased reactive oxygen species (ROS) and DNA damage and caused apoptosis in GH3 cells. T-2 toxin induced abnormal cell morphology, cytoplasm and nuclear shrinkage, nuclear fragmentation and formation of apoptotic bodies and autophagosomes. The mitochondrial degradative morphologies included local or total cristae collapse and small condensed mitochondria. T-2 toxin decreased the mitochondrial membrane potential. However, T-2 toxin significantly increased the superoxide dismutase (SOD) activity and expression of antioxidant genes glutathione peroxidase 1 (GPx-1), catalase (CAT), mitochondria-specific SOD-2 and mitochondrial uncoupling protein-1, -2 and -3 (UCP-1, 2 and 3). Interestingly, T-2 toxin increased adenosine triphosphate (ATP) levels and mitochondrial complex I activity, and increased the expression of most of mitochondrial electron transport chain subunits tested and critical transcription factors controlling mitochondrial biogenesis and mitochondrial DNA transcription and replication. T-2 toxin increased mitophagic activity by increasing the expression of mitophagy-specific proteins NIP-like protein X (NIX), PTEN-induced putative kinase protein 1 (PINK1) and E3 ubiquitin ligase Parkin. T-2 toxin activated the protective protein kinase A (PKA) signaling pathway, which activated the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/PINK1/Parkin pathway to mediate mitophagy. Taken together, our results suggested that the mammalian cells could increase their resistance against T-2 toxin by increasing the antioxidant activity, mitophagy and mitochondrial function.

KEYWORDS:

Antioxidant; Apoptosis; Mitochondria; Mitophagy; PGC-1; ROS

PMID:
29870751
DOI:
10.1016/j.toxlet.2018.05.041
[Indexed for MEDLINE]
Icon for Elsevier Science
6.
Domest Anim Endocrinol. 2018 Jul;64:77-83. doi: 10.1016/j.domaniend.2018.04.002. Epub 2018 Apr 10.

Influence of brain plasmalogen changes on gonadotropin secretion from the cultured bovine anterior pituitary cells.

Author information

1
Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi-shi, Yamaguchi-ken, 1677-1, Japan.
2
Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi-shi, Yamaguchi-ken, 1677-1, Japan. Electronic address: hiroya@yamaguchi-u.ac.jp.

Abstract

We recently discovered that the orphan G-protein-coupled receptor (GPR) 61 colocalized with GnRH receptors (GnRHRs) on the surface of most of bovine gonadotrophs. A recent study suggested that ethanolamine plasmalogen (PI) is a ligand for GPR61 in mouse neuroblastoma. Therefore, this study evaluated the hypothesis that PI alters LH and FSH secretion from cultured bovine anterior pituitary (AP) cells. We prepared bovine AP cells from postpubertal heifers (26 mo old) and cultured the cells for 3.5 d. We treated the cells with increasing concentrations (0, 5, 50, 500, 5,000, 50,000, or 500,000 pg/mL) of phosphoethanolamine PI (PEPI) extracted from the bovine brain, or l-α-lysophosphatidylethanolamine PI (LEPI) extracted from the bovine brain, for 5 min before either no treatment or GnRH stimulation. The medium samples were harvested 2 h after culture for LH and FSH assays. Phosphoethanolamine PI (50-500 pg/mL) stimulated (P < 0.05) the basal secretion of FSH but not LH. Phosphoethanolamine PI at 50 pg/mL also enhanced (P < 0.05) GnRH-induced FSH secretion. However, higher doses (500-500,000 pg/mL) of PEPI suppressed GnRH-induced FSH secretion. Moreover, 50 to 500,000 pg/mL PEPI suppressed GnRH-induced LH secretion. None of the tested concentrations of LEPI showed any effect on basal or GnRH-induced LH or FSH secretion. Pretreatment with Sma and Mad pathway inhibitors suppressed FSH secretion induced by PEPI, whereas an extracellular signal-regulated kinase pathway inhibitor blocked the PEPI-induced suppression of GnRH-stimulated LH secretion. Therefore, PEPI, but not LEPI, extracted from the bovine brain, alters FSH and LH secretion from cultured AP cells. Further studies are required to decide whether PEPI binds to GPR61 and whether PEPI plays an important role in the control of gonadotropin secretion from gonadotrophs.

KEYWORDS:

ERK; Ethanolamine plasmalogen; GPR61; Gonadotroph; SMAD

PMID:
29754010
DOI:
10.1016/j.domaniend.2018.04.002
[Indexed for MEDLINE]
Icon for Elsevier Science
7.
PLoS One. 2018 Apr 23;13(4):e0196029. doi: 10.1371/journal.pone.0196029. eCollection 2018.

Differentiation capacities of PS-clusters, adult pituitary stem/progenitor cell clusters located in the parenchymal-niche, of the rat anterior lobe.

Author information

1
Division of Life Science, Graduate School of Agriculture, Meiji University, Kanagawa, Japan.
2
Organization for the Strategic Coordination of Research and Intellectual Property, Meiji University, Kanagawa, Japan.
3
Institute of Reproduction and Endocrinology, Meiji University, Kanagawa, Japan.
4
Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
5
Department of Life Science, School of Agriculture, Meiji University, Kanagawa, Japan.
6
Laboratory of Anatomy and Cell Biology, Department of Health Sciences, Kyorin University, Tokyo, Japan.

Abstract

Pituitary endocrine cells are supplied by Sox2-expressing stem/progenitor cells in the anterior lobe of the adult pituitary. In relation to their microenvironment ("niche"), SOX2-positive cells exist in two types of niches; the marginal cell layer-niche and the parenchymal-niche. Recently, we isolated dense stem/progenitor cell clusters from the parenchymal-niche as parenchymal stem/progenitor cell (PS)-clusters. We classified these PS-clusters into three subtypes based on differences in S100β-expression (S100β-positive, -negative, and -mixed type), and reported that S100β-positive PS-clusters exhibited the capacity for differentiation into endocrine cells under 3-dimensional cultivation system. In the present study, we further characterized S100β-positive PS-clusters using an in vitro 2-dimensional cultivation system. The results demonstrated that S100β-positive PS-clusters in the 2-dimensional cultivation system proliferated more actively than S100β-negative clusters. Moreover, in 2-dimensional cultivation conditions, S100β-positive PS-clusters showed differentiation capacity into non-endocrine cells (Myogenin-, αSMA-, NG2-, or SOX17-positive cells) but not into endocrine cells, whereas S100β-negative PS-clusters did not. Collectively, PS-clusters were heterogeneous, exhibiting different proliferation and differentiation properties based on the difference in S100β-expression. Specifically, a part of SOX2-positive cells in the parenchymal-niche had capacities for differentiation into non-endocrine cells, and S100β-positive PS-clusters may be in more progressive stages toward differentiation than S100β-negative clusters.

PMID:
29684040
PMCID:
PMC5912746
DOI:
10.1371/journal.pone.0196029
[Indexed for MEDLINE]
Free PMC Article
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8.
Biomed Pharmacother. 2018 Jun;102:494-501. doi: 10.1016/j.biopha.2018.02.003. Epub 2018 Mar 24.

Bu-shen-zhu-yun decoction promotes synthesis and secretion of FSHβ and LHβ in anterior pituitary cells in vitro.

Author information

1
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China. Electronic address: jiangxiaofei78@163.com.
2
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China; Jiangsu Provincial Hospital of Traditional Chinese Medicine, China. Electronic address: zhouhuifang2011301@163.com.
3
Department of Obstetrics and Gynecology, Lishui Hospital of Traitional Chinese Medicine, Lishui, Zhejiang, 323000, China. Electronic address: 936391460@qq.com.
4
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China. Electronic address: 263522575@qq.com.
5
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China. Electronic address: 956030454@qq.com.
6
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China. Electronic address: 1335499687@qq.com.
7
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China; Pediatric Institution of Nanjing University of Chinese Medicine, Nanjing 210023, China. Electronic address: dfsjj@163.com.
8
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China; Pediatric Institution of Nanjing University of Chinese Medicine, Nanjing 210023, China. Electronic address: 710735592@qq.com.
9
The First Clinical College, Nanjing University of Chinese Medicine, Xianlin Road, Nanjing, Jiangsu Province, 210023, China; Pediatric Institution of Nanjing University of Chinese Medicine, Nanjing 210023, China. Electronic address: sunnyxyl1021@163.com.

Abstract

Luteal phase defects (LPD) are an important etiology of infertility which has increased in recent years. Studies have shown that bu-shen-zhu-yun decoction (BSZY-D) can lower the expression of estrogen receptor and progesterone receptor, in rats endometrium of embryonic implantation period, which upregulated by mifepristone, and improve uterine receptivity. The aim of present study was to determine the effect of BSZY-D on the synthesis and secretion of gonadotropic hormones in the anterior pituitary cells of rats. Rats were treated with saline (control) or BSZY-D two times/day for three estrous cycles by gavage. The cerebrospinal fluid (CSF) were collected for further cell treatment. The components in BSZY-D, serum and CSF were analysed by High Performance Liquid Chromatography (HPLC). Cells were either pretreated with normal CSF or BSZY-D/CSF before being stimulated with or without cetrorelix. The mRNA and proteins levels of receptors, hormones, and transcription factors were detected by RT-PCR, western blot analysis and immunostaining. We show that non-toxic concentrations of cetrorelix, a GnRH antagonist, can reduce the mRNA and protein levels of GnRHR, LH, and FSH. This effect could be reversed by the addition of BSZY-D/CSF. We also show decreased mRNA and protein expression of transcription factors, such as CREB, and Egr-1 and secretory vescicles, including SNAP-25 and Munc-18 upon treatment with cetrorelix could be reversed post co-treatment with BSZY-D/CSF. These results indicate that BSZY-D/CSF treatment led to increased levels of GnRHR, transcription factors, and secretory vesicles leading to increased secretion of FSH and LH. Thus, BSZY-D presents a promising candidate to treat luteal phase defects and infertility.

KEYWORDS:

Anterior pituitary cells; Bu-shen-zhu-yun decoction; FSH; Infertility; LH

PMID:
29579710
DOI:
10.1016/j.biopha.2018.02.003
[Indexed for MEDLINE]
Icon for Elsevier Science
9.
Eur J Clin Invest. 2018 Jun;48(6):e12927. doi: 10.1111/eci.12927. Epub 2018 Apr 16.

Clock genes alterations and endocrine disorders.

Author information

1
Department of Pathophysiology, Endocrine Unit, Laiko Hospital, National and Kapodistrian University of Athens, Athens, Greece.
2
Department of Biochemistry, National and Kapodistrian University of Athens, Athens, Greece.
3
Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK.
4
Division of Translational and Experimental Medicine, Warwick Medical School, University of Warwick, Coventry, UK.
5
Centre for Applied Biological & Exercise Sciences, Coventry University, Coventry, UK.
6
1st Department of Propaedeutic Internal Medicine, Medical School, Laikon Hospital, National and Kapodistrian University of Athens, Athens, Greece.

Abstract

BACKGROUND:

Various endocrine signals oscillate over the 24-hour period and so does the responsiveness of target tissues. These daily oscillations do not occur solely in response to external stimuli but are also under the control of an intrinsic circadian clock.

DESIGN:

We searched the PubMed database to identify studies describing the associations of clock genes with endocrine diseases.

RESULTS:

Various human single nucleotide polymorphisms of brain and muscle ARNT-like 1 (BMAL1) and Circadian Locomotor Output Cycles Kaput (CLOCK) genes exhibited significant associations with type 2 diabetes mellitus. ARNTL2 gene expression and upregulation of BMAL1 and PER1 were associated with the development of type 1 diabetes mellitus. Thyroid hormones modulated PER2 expression in a tissue-specific way, whereas BMAL1 regulated the expression of type 2 iodothyronine deiodinase in specific tissues. Adrenal gland and adrenal adenoma expressed PER1, PER2, CRY2, CLOCK and BMAL1 genes. Adrenal sensitivity to adrenocorticotrophin was also affected by circadian oscillations. A significant correlation between the expression of propio-melanocorticotrophin and PER 2, as well as between prolactin and CLOCK, was found in corticotroph and lactosomatotroph cells, respectively, in the pituitary. Clock genes and especially BMAL1 showed an important role in fertility, whereas oestradiol and androgens exhibited tissue-specific effects on clock gene expression. Metabolic disorders were also associated with circadian dysregulation according to studies in shift workers.

CONCLUSIONS:

Clock genes are associated with various endocrine disorders through complex mechanisms. However, data on humans are scarce. Moreover, clock genes exhibit a tissue-specific expression representing an additional level of regulation. Their specific role in endocrine disorders and their potential implications remain to be further clarified.

KEYWORDS:

PER ; adrenal; brain and muscle ARNT-like 1; circadian locomotor output cycles kaput; cryptochrome; diabetes mellitus; thyroid

PMID:
29577261
DOI:
10.1111/eci.12927
[Indexed for MEDLINE]
Icon for Wiley
10.
Ecotoxicol Environ Saf. 2018 Jul 30;156:116-124. doi: 10.1016/j.ecoenv.2018.03.029. Epub 2018 Mar 14.

Hypothalamic-pituitary-ovarian axis perturbation in the basis of bisphenol A (BPA) reproductive toxicity in female zebrafish (Danio rerio).

Author information

1
Departamento de Farmacología, Toxicología y Medicina Legal y Forense, Facultad de Veterinaria, Universidad de Córdoba, Campus de Rabanales, Edificio Darwin, 14071 Córdoba, Spain. Electronic address: ft2moloa@uco.es.
2
Departamento de Bioquímica y Biología Molecular, Campus de Excelencia Internacional Agroalimentario CeiA3, Universidad de Córdoba, Campus de Rabanales, Edificio Severo Ochoa, 14071 Córdoba, Spain.
3
Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Córdoba, Campus de Rabanales, Edificio de Sanidad Animal, 14071 Córdoba, Spain.
4
Departamento de Farmacología, Toxicología y Medicina Legal y Forense, Facultad de Veterinaria, Universidad de Córdoba, Campus de Rabanales, Edificio Darwin, 14071 Córdoba, Spain.

Abstract

Thousands of safety-related studies have been published on bisphenol A (BPA), an ubiquitous environmental pollutant with estrogenic activity and many other potential biological effects. In recent years, BPA exposure has been shown to cause anovulation and infertility through irreversible alteration of the hypothalamic-pituitary-gonadal axis in several organisms, including fish and mammals. Recently, the European Chemical Agency classified BPA as a "substance of very high concern" because of its endocrine-disrupting properties, which have serious effects on human health. Given the risk of exposure to BPA as a pollutant in the environment, food, and drinking water, the objective of our study was to assess the effects of this compound on the adeno-hypophysis by means of a histopathological and morphometric study of the gonadotroph cells. In addition, using quantitative real-time PCR (qRT-PCR) assays, we analyzed the changes in the expression of Cyp19b (an aromatase gene). Zebrafish were randomly distributed into five groups: a control group and 4 treated groups which were exposed to different BPA concentrations (1, 10, 100 and 1000 µg/L). The effects of the different doses on Cyp19b mRNA molecules followed a non-monotonic curve, with the 1 and 1000 µg/L doses causing dramatic decreases in the number of Cyp19b transcripts while the doses of 10 and 100 µg/L caused important increases. The consequences might be deregulation of gonadotropic hormones causing degeneration of gonadotropic cells, as observed in BPA treated animals. This is the first study in which the gonadotroph cells have been evaluated using histomorphological endpoints after BPA exposure in zebrafish.

KEYWORDS:

Adeno-hypophysis; Cyp19b; Endocrine-disrupting chemical; Fish; Gonadotroph cell

PMID:
29549734
DOI:
10.1016/j.ecoenv.2018.03.029
[Indexed for MEDLINE]
Icon for Elsevier Science
11.
PLoS One. 2018 Mar 13;13(3):e0194300. doi: 10.1371/journal.pone.0194300. eCollection 2018.

Regulation of FSH expression by differentially expressed miR-186-5p in rat anterior adenohypophyseal cells.

Author information

1
Department of Laboratory Animals, College of Animal Sciences, Jilin University, Changchun, Jilin, P.R. China.

Abstract

Follicle-stimulating hormone (FSH) has key roles in animal reproduction, including spermatogenesis and ovarian maturation. Many factors influence FSH secretion. However, despite the broad functions of microRNAs (miRNAs) via the regulation of target genes, little is known about their roles in FSH secretion. Our previous results suggested that miR-186-5p targets the 3' UTR of FSHb; therefore, we examined whether miR-186-5p could regulate FSH secretion in rat anterior adenohypophyseal cells. miR-186-5p was transfected into rat anterior pituitary cells. The expression of FSHb and the secretion of FSH were examined by RT-qPCR and ELISA. A miR-186-5p mimic decreased the expression of FSHb compared with expression in the control group and decreased FSH secretion. In contrast, both the mRNA levels and secretion of FSH increased in response to miR-186-5p inhibitors. Our results demonstrate that miR-186-5p regulates FSH secretion by directly targeting the FSHb 3' UTR, providing additional functional evidence for the importance of miRNAs in the regulation of animal reproduction.

PMID:
29534107
PMCID:
PMC5849326
DOI:
10.1371/journal.pone.0194300
[Indexed for MEDLINE]
Free PMC Article
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12.
Pituitary. 2018 Aug;21(4):443. doi: 10.1007/s11102-018-0879-1.

Immunohistochemistry for transcription factor T-Pit as a tool in diagnostics of corticotroph pituitary tumours.

Author information

1
Uppsala University, Uppsala, Sweden. olivera.casar-borota@igp.uu.se.
2
University of Oslo, Oslo, Norway.
3
Uppsala University, Uppsala, Sweden.

Comment on

PMID:
29468382
DOI:
10.1007/s11102-018-0879-1
[Indexed for MEDLINE]
Icon for Springer
13.
Tissue Cell. 2018 Feb;50:96-103. doi: 10.1016/j.tice.2017.12.008. Epub 2017 Dec 27.

Nintedanib effects on delaying cancer progression and decreasing COX-2 and IL-17 in the prostate anterior lobe in TRAMP mice.

Author information

1
Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), São Paulo, Brazil.
2
Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), São Paulo, Brazil. Electronic address: quitete@unicamp.br.

Abstract

Prostate cancer is the most prevalent type of cancer in men around the world. Due to its high incidence, new therapies have been evaluated, including drugs capable of inhibiting the FGF/VEGF pathways, as Nintedanib. The aim herein was to evaluate the Nintedanib therapeutic effects on morphology and COX-2 and IL-17 levels in the prostate anterior lobe in different grades of the tumor progression in TRAMP mice. Animals were treated with Nintedanib at a dose of 10 mg/kg/day in initial and intermediate grades of tumor development. At the end of treatment, the prostate anterior lobe was collected and submitted to morphological, immunohistochemical and Western Blotting analyses. The results showed that Nintedanib delayed the prostate carcinogenesis progression, with over 20% of reduction in frequency of tissue injuries, particularly in the group treated from 12 to 16 weeks of age. Also, decreased COX-2 and IL-17 levels were observed in both groups treated with Nintedanib in the prostate anterior lobe. Thus, we concluded that Nintedanib was effective in delaying tumor progression and, despite not directly acting on inflammation, Nintedanib may adversely affect inflammatory pathways, favoring prostate cancer delay.

KEYWORDS:

COX-2; IL-17; Inflammation; Nintedanib; Prostate cancer; TRAMP

PMID:
29429524
DOI:
10.1016/j.tice.2017.12.008
[Indexed for MEDLINE]
Icon for Elsevier Science
14.
Eur J Obstet Gynecol Reprod Biol. 2018 Mar;222:166-170. doi: 10.1016/j.ejogrb.2018.01.034. Epub 2018 Jan 31.

Diurnal rhythm of follicle-stimulating hormone is associated with nonalcoholic fatty liver disease in a Chinese elderly population.

Author information

1
Department of Geriatric Medicine, Fujian Provincial Hospital, Fujian Provincial Institute of Clinical Geriatrics, Fujian Provincial Key Laboratory of Geriatric Diseases, Fujian Medical University, Fuzhou, 350001, China.
2
Department of Pathology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, 350001, China.
3
Department of Geriatric Medicine, Fujian Provincial Hospital, Fujian Provincial Institute of Clinical Geriatrics, Fujian Provincial Key Laboratory of Geriatric Diseases, Fujian Medical University, Fuzhou, 350001, China. Electronic address: zpl7755@126.com.
4
Department of Endocrinology, Fujian Provincial Hospital Key Laboratory of Endocrinology, Fujian Medical University, Fuzhou, 350001, China. Electronic address: chengangfj@163.com.

Abstract

OBJECTIVE:

Previous studies have found that impairment of the circadian clock appears to contribute to the development of nonalcoholic fatty liver disease (NAFLD) and the circulating follicle-stimulating hormone (FSH) level showed a diurnal cycle. A recent study reported that a lower FSH level was associated with NAFLD. However, the effects of the diurnal rhythm of FSH on NAFLD have not been reported. The aim of this study was to evaluate whether the diurnal rhythm of FSH was associated with NAFLD in an elderly population.

STUDY DESIGN:

We performed a cross-sectional study among 71 elderly patients between August 2015 and November 2015 at Fujian Provincial Hospital. Anthropometrics and tests for laboratory were performed for each patient. FSH was determined by radioimmunoassay. The FSH receptor (FSHR) expression was identified in liver and ovary tissue by immunohistochemical staining. NAFLD was diagnosed by sonographic features.

RESULTS:

Of the 71 patients, 33 (42.9%) had NAFLD on their ultrasound. There were no significant differences between subjects with NAFLD and those without NAFLD in terms of age, sex, body mass index, waist-to-hip ratio, fasting plasma glucose, postload plasma glucose, liver enzyme, triglycerides, total cholesterol, high-density lipoprotein-cholesterol and low-density lipoprotein-cholesterol. Both the serum FSH levels of 8AM and 0AM showed no differences between the groups. The proportion of the 'normal' diurnal rhythm of FSH was higher among the patients with NAFLD (78.1% vs. 52.6%, P = .027). After adjusting for all potential confounders, the fully adjusted odds ratios (OR) of diurnal rhythm of FSH for NAFLD was 3.86 (95%CI: 1.01, 14.81, P = .049). Immunohistochemical staining showed that the FSHR protein was detected in human ovarian and hepatic tissues.

CONCLUSIONS:

These results suggest that the 'normal' diurnal rhythm of FSH was independently associated with NAFLD in an elderly population. This study provides a novel insight into the diurnal rhythm of FSH in the pathogenesis of NAFLD.

KEYWORDS:

Diurnal rhythm; Follicle-stimulating hormone (FSH); Nonalcoholic fatty liver disease (NAFLD)

PMID:
29408750
DOI:
10.1016/j.ejogrb.2018.01.034
[Indexed for MEDLINE]
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15.
G3 (Bethesda). 2018 Mar 2;8(3):859-873. doi: 10.1534/g3.117.300508.

Anterior Pituitary Transcriptome Suggests Differences in ACTH Release in Tame and Aggressive Foxes.

Author information

1
Department of Animal Sciences, College of Agriculture, Consumer, and Environmental Sciences, University of Illinois at Urbana-Champaign, Illinois 61801 jphekman@arborius.net avk@illinois.edu.
2
Department of Animal Sciences, College of Agriculture, Consumer, and Environmental Sciences, University of Illinois at Urbana-Champaign, Illinois 61801.
3
Department of Molecular and Integrative Physiology, School of Molecular and Cellular Biology, College of Liberal Arts and Sciences, University of Illinois at Urbana-Champaign, Illinois 61801.
4
Institute of Cytology and Genetics of the Russian Academy of Sciences, Novosibirsk 630090, Russia.
5
Program in Ecology, Evolution, and Conservation Biology, College of Liberal Arts and Sciences, University of Illinois at Urbana-Champaign, Illinois 61801.
6
Baker Institute for Animal Health, Cornell University, College of Veterinary Medicine, Ithaca, New York 14853.

Abstract

Domesticated species exhibit a suite of behavioral, endocrinological, and morphological changes referred to as "domestication syndrome." These changes may include a reduction in reactivity of the hypothalamic-pituitary-adrenal (HPA) axis and specifically reduced adrenocorticotropic hormone release from the anterior pituitary. To investigate the biological mechanisms targeted during domestication, we investigated gene expression in the pituitaries of experimentally domesticated foxes (Vulpes vulpes). RNA was sequenced from the anterior pituitary of six foxes selectively bred for tameness ("tame foxes") and six foxes selectively bred for aggression ("aggressive foxes"). Expression, splicing, and network differences identified between the two lines indicated the importance of genes related to regulation of exocytosis, specifically mediated by cAMP, organization of pseudopodia, and cell motility. These findings provide new insights into biological mechanisms that may have been targeted when these lines of foxes were selected for behavior and suggest new directions for research into HPA axis regulation and the biological underpinnings of domestication.

KEYWORDS:

RNA-seq; Vulpes vulpes; domestication; hypothalamic-pituitary-adrenal axis; pituitary

PMID:
29378821
PMCID:
PMC5844307
DOI:
10.1534/g3.117.300508
[Indexed for MEDLINE]
Free PMC Article
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16.
Endocrinology. 2018 Feb 1;159(2):1074-1087. doi: 10.1210/en.2017-00638.

Induction of Stress Signaling In Vitro and Suppression of Gonadotropin Secretion by Free Fatty Acids in Female Mouse Gonadotropes.

Author information

1
Department of Reproductive Medicine, University of California, San Diego, La Jolla, California.
2
Neonatal Intensive Care Unit, Dongguan Eighth People's Hospital, Dongguan, People's Republic of China.

Abstract

An emerging body of evidence supports the concept that the pituitary is a site for integration of multiple physiological and metabolic signals that inform and modulate endocrine pathways. Multiple endocrine mediators of energy balance and adiposity are known to impinge on the neuroendocrine axis regulating reproduction. Observations in humans show that obesity is correlated with decreased gonadotropin secretion, and studies have also suggested that pituitary sensitivity to stimulation by gonadotropin-releasing hormone (GnRH) is decreased in obese individuals. Free fatty acids are a potential mediator of adiposity and energy balance, but their impact as an endocrine modulator of pituitary function has not been closely examined. We evaluated the impact of free fatty acids on a pituitary gonadotrope cell line and in primary pituitary cultures of female mice. We show that increasing physiologically relevant doses of the monounsaturated ω-9 fatty acid oleate induces cellular stress and increases production of reactive oxygen species in a mouse gonadotrope cell line. In contrast, the unsaturated ω-3 α-linolenic and ω-6 linoleic fatty acids do not have this effect. Additionally, oleate can activate immediate-early gene expression independent of GnRH stimulation but has a negative impact on GnRH induction and expression of the gonadotropin subunit gene Lhb. Further, oleate suppresses gonadotropin secretion in response to pulsatile stimulation by GnRH. These results indicate that free fatty acids can directly alter gonadotropin gene expression and secretion in response to GnRH and may provide a link between energy sensing and reproduction.

PMID:
29315384
PMCID:
PMC5793794
[Available on 2019-02-01]
DOI:
10.1210/en.2017-00638
[Indexed for MEDLINE]
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17.
Toxicol Lett. 2018 Mar 15;285:104-112. doi: 10.1016/j.toxlet.2018.01.002. Epub 2018 Jan 3.

Differential regulation of tefluthrin and telmisartan on the gating charges of INa activation and inactivation as well as on resurgent and persistent INa in a pituitary cell line (GH3).

Author information

1
Department of Anesthesia, An Nan Hospital, China Medical University, 70965, Tainan City, Taiwan; Department of Anesthesia, China Medical University, 40447 Taichung City, Taiwan. Electronic address: d11320@mail.tmanh.org.tw.
2
Department of Physiology, National Cheng Kung University Medical College, 70101 Tainan City, Taiwan. Electronic address: snwu@mail.ncku.edu.tw.
3
Department of Pharmacology, College of Medicine, Kaohsiung Medical University, 80756 Kaohsiung City, Taiwan. Electronic address: yichlo@kmu.edu.tw.
4
Department of Medicine, Shanghai Medical College, Fudan University, Shanghai City, China. Electronic address: 15301056039@fudan.edu.cn.

Abstract

Voltage-gated Na+ currents (INa), known to contain many components (e.g., transient, resurgent and persistent INa) with unique gating properties, are involved in the generation and propagation of action potentials in excitable cells. In this study, how tefluthrin (Tef), a synthetic pyrethoid, and telmisartan (TEL), blocker of angiotensin II receptors can perturb those components of INa was investigated. The presence of either Tef or TEL increased the values of the gating charges of INa involved in the activation (za) and inactivation (zi). Tef also increased the amplitude of resurgent INa (INa(R)) or persistent INa (INa(P)) in a pituitary cell line (GH3), while TEL produced minimal effects on them. Subsequent addition of either ranolazine (a blocker of late INa) or d-limonene (a monoterpene), could reverse the changes by TEL or Tef on za or zi. In SCN5A-expressing HEK293T cells, addition of Tef or TEL also increased the peak amplitude and the inactivation time constant of INa which was accompanied by the increased za value of INa. Taken together, the results indicated that Tef- or TEL-mediated changes in the gating kinetics of INa are linked to their actions on functional activity of neurons, neuroendocrine or endocrine cells.

KEYWORDS:

Tefluthrin; Telmisartan; Voltage-gated Na(+) current

PMID:
29306026
DOI:
10.1016/j.toxlet.2018.01.002
[Indexed for MEDLINE]
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18.
Pituitary. 2018 Apr;21(2):194-202. doi: 10.1007/s11102-017-0858-y.

Silent somatotroph pituitary adenomas: an update.

Author information

1
Department of Endocrinology, Centre hospitalier universitaire de Sherbrooke, Sherbrooke, QC, Canada.
2
Department of Medicine, Oregon Health & Science University, Portland, OR, USA.
3
Northwest Pituitary Center, Oregon Health & Science University, Portland, OR, USA.
4
Department of Pathology, Oregon Health & Science University, Portland, OR, USA.
5
Department of Neurological Surgery, Oregon Health & Science University, Portland, OR, USA.
6
Department of Neurological Surgery, Oregon Health & Science University, Portland, OR, USA. fleseriu@ohsu.edu.
7
Department of Medicine, Oregon Health & Science University, Portland, OR, USA. fleseriu@ohsu.edu.
8
Northwest Pituitary Center, Oregon Health & Science University, Portland, OR, USA. fleseriu@ohsu.edu.

Abstract

Silent growth hormone adenomas (SGHA) are a rare entity of non-functioning pituitary neuroendocrine tumors. Diagnosis is invariably made post-operatively of a tumor immunopositive for GH (and Pit-1 in selected cases) but without clinical acromegaly. Mainly young females are affected, and tumors are often uncovered by investigation for headaches or oligoamenorrhea. Integration of clinical, pathological and biochemical data is required for proper diagnosis. Beside normal IGF-1 levels, a third of SGHAs displays elevated GH levels and some will eventually progress to acromegaly. Almost two-thirds will be mixed GH-prolactin tumors and sparsely-granulated monohormonal GH tumors seems the more aggressive subtype. Recurrence and need for radiation is higher than other non-functioning tumors so close follow-up is warranted.

KEYWORDS:

Neuroendocrine tumors; Non-functioning pituitary adenomas; Pituitary; Silent somatotroph; Somatotroph adenomas

PMID:
29305680
DOI:
10.1007/s11102-017-0858-y
[Indexed for MEDLINE]
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19.
Endocrinology. 2018 Mar 1;159(3):1264-1276. doi: 10.1210/en.2017-00653.

Sex- and Age-Specific Impact of ERK Loss Within the Pituitary Gonadotrope in Mice.

Author information

1
Department of Biomedical Science, College of Veterinary Medicine, Cornell University, Ithaca, New York.
2
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana.
3
Experimental Pharmacology, Center for Molecular Signaling, Saarland University School of Medicine, Homburg, Germany.
4
Department of Pharmacology and Therapeutics, McGill University, Québec, Canada.

Abstract

Extracellular signal-regulated kinase (ERK) signaling regulates hormone action in the reproductive axis, but specific mechanisms have yet to be completely elucidated. In the current study, ERK1 null and ERK2 floxed mice were combined with a gonadotropin-releasing hormone receptor (GnRHR)-internal ribosomal entry site-Cre (GRIC) driver. Female ERK double-knockout (ERKdko) animals were hypogonadotropic, resulting in anovulation and complete infertility. Transcript levels of four gonadotrope-specific genes (GnRHR and the three gonadotropin subunits) were reduced in pituitaries at estrus in ERKdko females, and the postcastration response to endogenous GnRH hyperstimulation was blunted. As females aged, they exhibited abnormal ovarian histology, as well as increased body weight. ERKdko males were initially less affected, showing moderate subfertility, up to 6 months of age. Male ERKdko mice also displayed a blunted response to endogenous GnRH following castration. By 12 months of age, ERKdko males had reduced testicular weights and sperm production. By 18 months of age, the ERKdko males displayed reduced testis and seminal vesicle weights, marked seminiferous tubule degeneration, and a 77% reduction in sperm production relative to controls. As the GRIC is also active in the male germ line, we examined the specific role of ERK loss in the testes using the stimulated by retinoic acid 8 (Stra8)-Cre driver. Whereas ERK loss in GRIC and Stra8 males resulted in comparable losses in sperm production, seminiferous tubule histological degeneration was only observed in the GRIC-ERKdko animals. Our data suggest that loss of ERK signaling and hypogonadotropism within the reproductive axis impacts fertility and gonadal aging.

PMID:
29300908
PMCID:
PMC5802804
[Available on 2019-03-01]
DOI:
10.1210/en.2017-00653
[Indexed for MEDLINE]
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20.
Usp Fiziol Nauk. 2017 Jan-Mar;48(1):80-90.

Sensitivity of T-Lymphocytes to Hormones of the Anterior Pituitary Gland.

[Article in Russian]

Abstract

The review provides information about the features of the sensitivity of thymocytes, lymphoid organs' cells and T-lymphocytes of peripheral blood to the hormones secreted by anterior pituitary gland's cells: growth hormone, thyrotropin, adrenocorticotropic hormone, prolactin and β-endorphin. Some aspects of the T-lymphocytes's response to humoral signals from the hypophysis are shown in the article. Also the pituitary hormones' role in the regulation of proliferation, differentiation, and cytokine production of T-lymphocytes in normal and pathological conditions of the organism being discussed.

PMID:
29283520
[Indexed for MEDLINE]

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