Elevated expression of urotensin II and its receptor in diabetic cardiomyopathy

Abstract Objective Urotensin II (UII) is a somatostatin-like peptide recently identified to have several cardiovascular effects, including potent vasoactive, cardiac inotropic and chronotropic properties. Our aim was to determine the degree of expression of UII and UII receptor (UT) in the myocardiu...

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Bibliographic Details
Published in:Journal of diabetes and its complications 2008-03, Vol.22 (2), p.137-143
Main Authors: Dai, Hong-Yan, Guo, Xin-Gui, Ge, Zhi-Ming, Li, Zhen-Hua, Yu, Xiao-Jing, Tang, Meng-Xiong, Zhang, Yun
Format: Article
Language:English
Subjects:
Animals
Cardiac remodeling
Cardiomyocytes
Diabetes
Diabetes Mellitus, Experimental - genetics
Diabetic Angiopathies - genetics
Diabetic Angiopathies - pathology
Diabetic cardiomyopathy
Endocrinology & Metabolism
Endothelium
Gene Expression Regulation
Glucose
Heart Diseases - genetics
Heart Diseases - pathology
Insulin resistance
Male
Mortality
Myocardium - pathology
Pathogenesis
Peptides
Proteins
Rats
Rats, Wistar
Receptors, G-Protein-Coupled - genetics
Reverse Transcriptase Polymerase Chain Reaction
Rodents
Smooth muscle
Urotensin II
Urotensins - genetics
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Summary:Abstract Objective Urotensin II (UII) is a somatostatin-like peptide recently identified to have several cardiovascular effects, including potent vasoactive, cardiac inotropic and chronotropic properties. Our aim was to determine the degree of expression of UII and UII receptor (UT) in the myocardium of rats with streptozotocin (STZ)-induced diabetes. Methods Real-time polymerase chain reaction, Western blot, and immunohistochemistry were used to determine the degree of expression and location of UII and UT in the myocardium of STZ-induced diabetic rats. Results UII and UT expression were significantly enhanced in the myocardium of rats with diabetes compared with healthy controls on both messenger RNA and protein levels. Both UII and UT protein expression were mainly concentrated in the cardiomyocytes, endothelial cells, cardiac fibroblasts, and smooth muscle cells of diabetic cardiomyopathy (DCM). Conclusions Our results suggest a possible role for the UII/UT system in the pathophysiology of DCM.
ISSN:1056-8727
1873-460X
DOI:10.1016/j.jdiacomp.2006.10.008