Abstract
Previous studies in our laboratory have demonstrated a sexual dimorphism in the response to balloon injury of the rat carotid artery, with marked attenuation in neointima formation in females compared with males. 1 Chen S.J. Li H. Durand J. Oparil S. Chen Y.F. Estrogen reduces myointimal proliferation after balloon injury of the rat carotid artery. Circulation. 1996; 93: 577-584 Crossref PubMed Scopus (221) Google Scholar Subsequent investigations established that this sexual dimorphism is estrogen dependent, because daily systemic administration of 17β-estradiol in a dose (20 μg/kg/day subcutaneously [SC]) that produced physiologic (20 to 50 pg/ml) levels of the circulating hormone attenuated neointima formation in gonadectomized rats of both sexes, whereas testosterone treatment had no effect. 2 Levine R.L. Chen S.J. Durand J. Chen Y.F. Oparil S. Medroxyprogesterone attenuates estrogen-mediated inhibition of neointima formation after balloon injury of the rat carotid artery. Circulation. 1996; 94: 2221-2227 Crossref PubMed Scopus (108) Google Scholar Many of the early molecular and/or cellular events in the vascular injury response exhibited sexual dimorphism and/or modulation by estrogen. For example, expression of the early response gene c-myc was increased >10-fold within 2 hours of balloon injury in the carotid artery of the male rat, but was minimally changed in the female. 1 Chen S.J. Li H. Durand J. Oparil S. Chen Y.F. Estrogen reduces myointimal proliferation after balloon injury of the rat carotid artery. Circulation. 1996; 93: 577-584 Crossref PubMed Scopus (221) Google Scholar More recent studies have shown that both vascular smooth muscle cells (VSMCs) and adventitial fibroblasts are activated and migrate toward the neointima within 24 to 72 hours of endoluminal injury of a rat carotid artery, and that these processes are modulated by estrogen. 3 Oparil S. Chen S.J. Chen Y.F. Durand J.N. Allen L. Thompson J.A. Estrogen attenuates the adventitial contribution to neointima formation in injured rat carotid arteries. Cardiovasc Res. 1999; 44: 608-614 Crossref PubMed Scopus (68) Google Scholar Based on these observations, we hypothesized that short-term systemic estrogen treatment beginning at the time of injury would attenuate the vascular injury response. The present study tested that hypothesis.
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