[Ghrelin stimulates in vitro angiogenic capacity of rat cardiac microvascular endothelial cells].

Autor:	Wang L; Department of Geriatrics Cardiology, Chongqing Medical University, Chongqing, China., Chen QW, Li GQ, Ke DZ
Jazyk:	čínština
Zdroj:	Zhonghua xin xue guan bing za zhi [Zhonghua Xin Xue Guan Bing Za Zhi] 2012 Jan; Vol. 40 (1), pp. 50-6.
Abstrakt:	Objective: To clarify whether ghrelin could promote in vitro rat cardiac microvascular endothelial cells (CMECs) angiogenesis and related mechanisms. Methods: CMECs were isolated from myocardial tissue of adult male SD rats and characterized by the immunocytochemistry staining with Factor VIII and the capacity of in vitro capillary tube-like formation. The mRNAs and protein expressions of ghrelin and its receptor (growth hormone secretagogue receptor, GHS-R) of CMECs were determined by RT-PCR, Immunofluorescence, ELISA and Western blot. Proliferation, migration and in vitro angiogenesis as well as ERK2 phosphorylation of CMECs were tested in the presence of ghrelin (10(-9) - 10(-7) mol/L) with or without pretreatment with specific MAPK/ERK2 inhibitor PD98059. Results: Purity of CMECs characterized by immunocytochemistry staining with Factor VIII was about 95%, and the cells showed a high ability to form the capillary tube-like structures on Matrigel. Ghrelin and GHS-R were constitutively expressed in CMECs. Proliferation, migration and in vitro angiogenesis capacities of CMECs (72.20 ± 5.72 vs. 28.60 ± 5.13, P < 0.001; 71.00 ± 7.78 vs. 28.60 ± 5.13, P < 0.001) as well as ERK2 phosphorylation (0.92 ± 0.13 vs. 0.29 ± 0.04, P < 0.001; 1.15 ± 0.16 vs. 0.29 ± 0.04, P < 0.001) were significantly enhanced by exogenous ghrelin (10(-8) - 10(-7) mol/L). PD98059 abolished ghrelin-induced ERK2 phosphorylation and in vitro angiogenesis. Conclusions: Ghrelin and its receptor are expressed in CMECs and ghrelin could stimulate CMECs in vitro angiogenesis through activation of MAPK/ERK2 signaling pathway.
Databáze:	MEDLINE
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