Effects of dehydroepiandrosterone on proliferation of human aortic smooth muscle cells

被引:39
作者
Yoneyama, A
Kamiya, Y
Kawaguchi, M
Fujinami, T
机构
[1] Third Dept. of Internal Medicine, Nagoya City Univ. Medical School, Nagoya 467, Mizuho-cho, Mizuho-ku
关键词
dehydroepiandrosterone; vascular smooth muscle; atherosclerosis; A10; cells;
D O I
10.1016/S0024-3205(97)00011-8
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) have been shown to be associated with the progression of coronary atherosclerosis in clinical and in vivo studies. However, the mechanisms responsible for the association have not been determined. In the present study, we found that DHEA influences the in vitro growth of vascular smooth muscle cells obtained from the human aorta (hASMC). The concentrations of DHEA ranging from 10(-8) M to 10(-6) M significantly stimulated the mitogenesis of hASMC in serum-free culture. On the other hand, 4 hrs of pretreatment with DHEA attenuated the fetal calf serum induced proliferative effect in a dose-dependent manner. However, the in vitro effects of DHEA on the mitogenesis observed in hASMC were not seen in rat-derived aortic smooth muscle cell lines (A10 cells). With respect to DHEAS, the hormone, at concentrations up to 10(-5) M did not affect the growth of either hASMC or A10 cells in vitro. The growth response of hASMC to DHEA in vitro was markedly affected by the culture conditions. The differential proliferative effects of DHEA on smooth muscle cells between rat and human are of interest. We conclude that the effects of DHEA on mitogenesis of hASMC may, at least in part, explain the association between DHEA and atherosclerosis.
引用
收藏
页码:833 / 838
页数:6
相关论文
共 16 条
[1]   DEHYDROEPIANDROSTERONE FEEDING PREVENTS AORTIC FATTY STREAK FORMATION AND CHOLESTEROL ACCUMULATION IN CHOLESTEROL-FED RABBIT [J].
ARAD, Y ;
BADIMON, JJ ;
BADIMON, L ;
HEMBREE, WC ;
GINSBERG, HN .
ARTERIOSCLEROSIS, 1989, 9 (02) :159-166
[2]  
CONNOR EB, 1986, NEW ENGL J MED, V315, P1519
[3]   INHIBITION OF ACCELERATED CORONARY ATHEROSCLEROSIS WITH DEHYDROEPIANDROSTERONE IN THE HETEROTOPIC RABBIT MODEL OF CARDIAC TRANSPLANTATION [J].
EICH, DM ;
NESTLER, JE ;
JOHNSON, DE ;
DWORKIN, GH ;
KO, D ;
WECHSLER, AS ;
HESS, ML .
CIRCULATION, 1993, 87 (01) :261-269
[4]   DECREASED TESTOSTERONE AND DEHYDROEPIANDROSTERONE-SULFATE CONCENTRATIONS ARE ASSOCIATED WITH INCREASED INSULIN AND GLUCOSE-CONCENTRATIONS IN NONDIABETIC MEN [J].
HAFFNER, SM ;
VALDEZ, RA ;
MYKKANEN, L ;
STERN, MP ;
KATZ, MS .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1994, 43 (05) :599-603
[5]   GLUCOCORTICOID INHIBITS CAMP PRODUCTION INDUCED BY VASOACTIVE AGENTS IN AORTIC SMOOTH-MUSCLE CELLS [J].
ITO, Y ;
KOZAWA, O ;
TOKUDA, H ;
SUZUKI, A ;
WATANABE, Y ;
KOTOYORI, J ;
OISO, Y .
ATHEROSCLEROSIS, 1994, 110 (01) :69-76
[6]   PHYSICOCHEMICAL CHARACTERIZATION OF [H-3] DHEA BINDING IN RAT-LIVER [J].
KALIMI, M ;
REGELSON, W .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 156 (01) :22-29
[7]   EFFECT OF SOMATOSTATIN AND ITS ANALOG ON PROLIFERATION OF HUMAN EPIDERMOID CARCINOMA-CELLS INVITRO [J].
KAMIYA, Y ;
OHMURA, E ;
ARAI, M ;
FUJII, T ;
HAYAKAWA, F ;
ITO, J ;
KAWAGUCHI, M ;
TSUSHIMA, T ;
SAKUMA, N .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1993, 191 (01) :302-307
[8]   HUMAN VASCULAR SMOOTH-MUSCLE CELLS CONTAIN FUNCTIONAL ESTROGEN-RECEPTOR [J].
KARAS, RH ;
PATTERSON, BL ;
MENDELSOHN, ME .
CIRCULATION, 1994, 89 (05) :1943-1950
[9]   DEHYDROEPIANDROSTERONE SULFATE, INCIDENCE OF MYOCARDIAL-INFARCTION, AND EXTENT OF ATHEROSCLEROSIS IN MEN [J].
LACROIX, AZ ;
YANO, K ;
REED, DM .
CIRCULATION, 1992, 86 (05) :1529-1535
[10]  
MAW RW, 1992, J STEROID BIOCH MOL, V42, P293