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ANGIOTENSIN II‐INDUCED GROWTH OF VASCULAR SMOOTH MUSCLE CELLS IS ASSOCIATED WITH MODULATION OF CELL SURFACE AREA AND PLATELET‐DERIVED GROWTH FACTOR RECEPTOR EXPRESSION
Author(s) -
Kuma Sosei,
Oki Eiji,
Onohara Toshihiro,
Komori Kimihiro,
Maehara Yoshihiko
Publication year - 2007
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04535.x
Subject(s) - vascular smooth muscle , angiotensin ii , platelet derived growth factor receptor , endocrinology , medicine , growth factor , receptor , platelet derived growth factor , cell growth , cell , platelet , biology , chemistry , microbiology and biotechnology , smooth muscle , biochemistry
SUMMARY1 Excessive growth of vascular smooth muscle cells (VSMC) can lead to critical problems in the treatment of some vascular diseases. Recent studies suggest a connection between this abnormal growth of VSMC and the octapeptide hormone angiotensin (Ang) II. However, the growth‐promotive potential of AngII on VSMC is unclear. 2 Using the novel AngII inhibitor E4177 and an original animal model, we confirmed that AngII does function in abnormal growth of VSMC induced after transplantation of vein grafts in an animal model. 3 Furthermore, using a primary culture of human aortic smooth muscle cells (HASMC), we found that AngII augmented the growth of HASMC in a serum‐dependent manner and induced enlargement of the cell surface area in HASMC, both effects being nullified by E4177. The latter effect of AngII was associated with an increase in the expression level of platelet‐derived growth factor (PDGF) receptors. In specimens obtained from the animal model, PDGF receptors were highly expressed. 4 These data obtained in vitro and in vivo imply that AngII has the potential to promote growth of VSMC and suggest that this growth promotion may be mediated by enlargement of the cell surface area.