Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (41): 7647-7652.doi: 10.3969/j.issn.1673-8225.2011.41.012

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Portosystemic collateral vessel and splanchnic vessel formation in a rat model of portal hypertension

Mao Xiao-Huan1, 2, Dai Wen-Jian1, Yang Li2, Liu Wei2   

  1. 1Hunan Environment and Biology Polytechnique College, Hengyang 421005, Hunan Province, China
    2Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China
  • Received:2011-02-26 Revised:2011-05-09 Online:2011-10-08 Published:2011-10-08
  • About author:Mao Xiao-huan, Lecturer, Hunan Environment and Biology Polytechnique College, Hengyang 421005, Hunan Province, China; Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China csumxh@sina.com
  • Supported by:

    the National Natural Science Foundation of China, No. 30901577*; the Scientific Research Foundation for Returned Overseas Chinese Scholars, State Education Ministry, No. 20091590*; a Grant from Education Department of Hunan Province No.11C0469*

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Abstract:

BACKGROUND: The Apelin/APJ system has been confirmed to decrease blood pressure, strengthen systole and Apelin can stimulate angiogenesis.
OBJECTIVE: To determine the expression of apelin and APJ in splanchnic tissues, and to test if apelin has a pathophysiological role in the development of splanchnic neovascularization, splanchnic hyperemia, and portosystemic collateralization in a rat model of portal hypertension.
METHODS: Partial portal vein-ligated rats were treated with the APJ antagonist F13A for 7 days. Splanchnic neovascularization and expression of angiogenesis mediators (western blotting) were determined. Portosystemic collateral formation (microspheres) and hemodynamic parameters (?ow cytometry) were also assessed.
RESULTS AND CONCLUSION: Apelin and its receptor APJ were overexpressed in the splanchnic vasculature of portal hypertensive rats. F13A effectively decreased, by 52%, splanchnic neovascularization and expression of proangiogenic factors vascular endothelial growth factor, platelet derived growth factor, and angiopoietin-2 in portal hypertensive rats. F13A also reduced, by 35%, the formation of portosystemic collateral vessels. These findings suggest that the apelin/APJ system contributes to portosystemic collateralization and splanchnic neovascularization in portal hypertensive rats, presenting a potential novel therapeutic target for portal hypertension.

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