We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 5

1.
Figure 2

Figure 2. From: Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities.

Elevated circulating HIF-inducible factors in PAH. Factors are grouped according to their biologic activity on stem cells/progenitors. Box plots indicate median values, upper and lower quartiles. Levels of erythropoietin are strongly related to HGF in PAH subjects.

Samar Farha, et al. Blood. 2011 March 31;117(13):3485-3493.
2.
Figure 4

Figure 4. From: Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities.

Increased circulating progenitor cells in nonaffected family members of patients with FPAH. Values of circulating progenitors in nonaffected family members were comparable with their afflicted family members. Single- and double-positive CD34 and CD133 cells were measured in circulation using flow cytometry. Box plots indicate median values, upper and lower quartiles.

Samar Farha, et al. Blood. 2011 March 31;117(13):3485-3493.
3.
Figure 5

Figure 5. From: Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities.

Pulmonary vascular disease and myeloid abnormalities in PAH. This study identifies hemangioblast proliferation and fibrosis as key components in the pathophysiology of PAH. Increased levels of HIF-inducible factors, some of which are produced by diseased pulmonary vascular cells, promote hemangioblast proliferation and progenitor cell mobilization. Local production of recruitment factors by pulmonary vascular endothelium attract mobilized progenitor cells into the pulmonary artery wall where these cells fuel vascular remodeling. (Illustration by David Schumick, BS, CMI. Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography, 2010. All rights reserved.)

Samar Farha, et al. Blood. 2011 March 31;117(13):3485-3493.
4.
Figure 3

Figure 3. From: Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities.

Increased production of HGF and SDF-1α by primary human pulmonary arterial endothelial cells (PAECs) from PAH. (A) HGF and SDF-1α is secreted by PAH PAEC in culture at higher levels than by control cells under both normoxia and hypoxia conditions (*all P < .05). HGF secretion by PAH PAEC was significantly increased on exposure to hypoxia (ANOVA P = .0001). SDF-1α levels also significantly increased with hypoxia in both PAH (ANOVA P = .0001) and control PAEC (ANOVA P = .0007). (B) HGF and SDF-1α in lung tissues from controls and PAH patients. Endothelial cells in plexiform lesions of PAH lungs had strong positive immunoreactivity for HGF (arrowheads identify endothelial cells lining vascular lumens). Endothelial cells of control lung expressed HGF, but immunopositivity was much less prominent (arrowheads). SDF-1α expression was present in endothelial cells of plexiform lesions in PAH lung (arrowheads). Only mild immunopositivity for SDF-1α was found in vessel endothelium of control lung (arrowheads). Scale bars: 40 μm.

Samar Farha, et al. Blood. 2011 March 31;117(13):3485-3493.
5.
Figure 1

Figure 1. From: Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities.

Greater CD34+CD133+ progenitors in PAH. (A-D) CD34+CD133+ progenitors in PAH determined by flow cytometry. Box plots indicate median values, upper and lower quartiles. There are increased hemangioblasts in PAH bone marrow, and higher levels of CD34+CD133+ progenitors in circulation and within the pulmonary artery endothelium than in controls. (E-F) STAT3 and STAT5 activation and localization in bone marrow biopsies. Cellular localization of phosphoSTAT3 (pSTAT3) by immunohistochemical staining in bone marrow biopsy (arrowheads) from PAH patient and healthy control (E). Immunohistochemical staining for phosphoSTAT5 (pSTAT5) in bone marrow biopsy (arrowheads) from PAH patient and healthy control (F). (G) Reticulin increase in bone marrow of PAH patients. Reticulin staining as a measure of myelofibrosis, was increased in PAH bone marrows. Arrowheads identify reticulin staining in bone marrow biopsies from PAH subject. The reticulin stain around a blood vessel is normally present, and is shown as internal positive in the control tissue. (H) EpoR expression by flow cytometry. Dashed lined histogram indicates background staining with isotype control antibodies, solid histogram indicates EpoR staining. CFU-EC have low levels of EpoR, while lymphocytes are shown as negative control have no EpoR. (I) STAT5 activation in CFU-EC. Electrophoretic mobility shift assay for STAT5 DNA binding activation in whole cell extract of CFU-EC from PAH patient (lane 4) and healthy control (lane 3) is shown. STAT5 DNA-binding activation is similar among PAH and control CFU-EC. A549 cells stimulated with Epidermal Growth Factor (EGF) is a positive control, and the supershift using antibody to STAT5 identifies the STAT5-DNA complex (arrow). Scale bars: 6 μm (E); 10 μm (F); 40 μm (G).

Samar Farha, et al. Blood. 2011 March 31;117(13):3485-3493.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk