Format

Send to

Choose Destination
See comment in PubMed Commons below
Peptides. 2014 Aug;58:91-7. doi: 10.1016/j.peptides.2014.06.001. Epub 2014 Jun 14.

Elevated adropin: a candidate diagnostic marker for myocardial infarction in conjunction with troponin-I.

Author information

1
Department of Cardiovascular Surgery, Elazig Research and Education Hospital, Elazig 23100, Turkey; Firat University, School of Medicine, Department of Anatomy, Elazig 23119, Turkey.
2
Firat University, School of Medicine, Department of Histology and Embryology, Elazig 23119, Turkey.
3
Firat University, School of Medicine, Department of Medical Biochemistry (Firat Hormones Research Group), Elazig 23119, Turkey. Electronic address: saydin1@hotmail.com.
4
Laboratory of Medical Biochemistry, Elazig Research and Education Hospital, Elazig 23100, Turkey; Department of Cardiology, Van Ercis State Hospital, Van, Turkey.
5
Firat University, School of Medicine, Department of Medical Biochemistry (Firat Hormones Research Group), Elazig 23119, Turkey.
6
Dicle University, School of Medicine, Department of Cardiovascular Surgery, Diyarbakir 21280, Turkey.

Abstract

Myocardial infarction (MI; "heart attack") can cause injury to or death of heart muscle tissue (myocardium) owing to prolonged ischemia and hypoxia. Troponins and CK-MB are released from heart muscle cells during MI. It has been demonstrated that energy expenditure is regulated by adropin expressed in the endocardium, myocardium, and epicardium. We hypothesized that adropin is released into the bloodstream during myocardial muscle injury caused by MI, so the serum level rises as myocytes die. Therefore, we examined the association between adropin expression and myocardial infarction in isoproterenol-induced myocardial infarction. Rats were randomly allocated to six groups. After treatment they were decapitated and their blood and tissues were collected for adropin measurement. Changes in adropin synthesis in rat heart, kidney and liver tissues in isoproterenol (ISO)-induced MI were demonstrated immunohistochemically. Serum adropin concentrations were measured by ELISA, and troponin-I, CK and CK-MB concentrations by autoanalysis. The results demonstrated that cardiac muscle cells, glomerular, peritubular and renal cortical interstitial cells, hepatocytes and liver sinusoidal cells all synthesize adropin, and synthesis increased 1-24 h after MI except in the liver cells. The findings elucidate the pathogenesis of MI, and the gradual increase in serum adropin could be a novel diagnostic marker and serve as an alternative to troponin-I measurement for diagnosing MI.

KEYWORDS:

Adropin; Cardiac muscle cells; Hepatocytes; Kidneys; Myocardial infarction

PMID:
24932661
DOI:
10.1016/j.peptides.2014.06.001
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center