Song J, Wan Y, Rolfe B E, Campbell J H, Campbell G R
Centre for Research in Vascular Biology, Department of Anatomical Sciences, University of Queensland, Brisbane, Australia.
Atherosclerosis. 1998 Sep;140(1):97-104. doi: 10.1016/s0021-9150(98)00122-1.
To investigate the growth-regulating action of estrogen on vascular smooth muscle cells (SMC), effects of beta-17-estradiol (beta-E2) on phenotypic modulation and proliferation of rabbit aortic SMC were observed in vitro. At 10(-8)M, beta-E2 significantly slowed the decrease in volume fraction of myofilaments (Vv myo) of freshly dispersed SMCs in primary culture, indicating an inhibitory effect of beta-E2 on spontaneous phenotypic modulation of SMC from a contractile to a synthetic phenotype. Freshly dispersed SMCs treated with beta-E2 also had a relatively longer quiescent phase than control cells before intense proliferation occurred. This was in contrast to SMCs in passage 2 3 (synthetic state), where beta-E2-treated cells replicated significantly faster than untreated cells. beta-E2 also markedly enhanced the serum-induced DNA synthesis of synthetic SMCs in a concentration-dependent manner within physiological range (10(-10)to 10(-8)M). These findings indicate that the growth-regulating effect of estrogen on vascular SMC is dependent on the cell's phenotypic state. It delays the cell cycle re-entry of the contractile SMCs by retarding their phenotypic modulation: however, once cells have modulated to the synthetic phenotype, it promotes their replication.
为研究雌激素对血管平滑肌细胞（SMC）的生长调节作用，体外观察了β-17-雌二醇（β-E2）对兔主动脉SMC表型调节和增殖的影响。在10^(-8)M时，β-E2显著减缓了原代培养中新鲜分散的SMC肌丝体积分数（Vv myo）的降低，表明β-E2对SMC从收缩型到合成型的自发表型调节具有抑制作用。用β-E2处理的新鲜分散的SMC在强烈增殖发生之前也比对照细胞具有相对更长的静止期。这与第2-3代SMC（合成状态）相反，在那里用β-E2处理的细胞比未处理的细胞复制明显更快。β-E2还在生理范围内（10^(-10)至10^(-8)M）以浓度依赖的方式显著增强血清诱导的合成型SMC的DNA合成。这些发现表明雌激素对血管SMC的生长调节作用取决于细胞的表型状态。它通过延迟其表型调节来延迟收缩型SMC的细胞周期重新进入；然而，一旦细胞已调节至合成型表型，它就会促进其复制。
