The effect of estradiol on the proliferation of rabbit aortic medial tissue culture cells induced by hyperlipemic serum

Fischer-Dzoga, Katti; Wissler, Robert W.; Vesselinovitch, Dragoslava

doi:10.1016/0014-4800(83)90064-3

Cited by 94 publications

(35 citation statements)

References 19 publications

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“…Evidence exists for the presence of estrogen 53 -58 and progesterone 58 receptors in arterial endothelial and smooth muscle cells in several mammalian species. Other studies have shown that estrogen treatment in vivo or in vitro is associated with reductions in arterial smooth muscle cell proliferation, 59 decreased collagen and elastin production, 60 -63 and increased degradation of collagen and elastin in arterial tissue. 64 Thus, evidence indicates that vascular estrogen receptors are physiologically functional, and, therefore, deficiencies in endogenous reproductive steroids may influence atherogenesis directly at the level of the artery wall.…”

Section: Discussionmentioning

confidence: 96%

Ovariectomy, social status, and atherosclerosis in cynomolgus monkeys.

Adams¹,

Kaplan²,

Clarkson³

et al. 1985

Arteriosclerosis

151

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Evidence is contradictory regarding the effects of natural or surgical menopause on "female protection" against coronary artery atherosclerosis. We evaluated atherosclerosis, plasma lipids, blood pressure, and carbohydrate tolerance in 21 ovariectomized and 23 intact female cynomolgus macaques fed a moderately atherogenic diet for 30 months. We also evaluated the influence of social dominance status, with particular emphasis on a possible relationship with ovarian endocrine function. Atherosclerosis was two to 10 times as extensive in coronary, carotid, and iliacofemoral arteries of the ovariectomized females; this could be explained, in part, by 15% to 20% increases in total plasma and LDL cholesterol concentrations. Socially dominant intact females were protected against advanced atherosclerotic lesions (plaques) of the coronary arteries, while subordinate females and ovariectomized females were not. Increased susceptibility to advanced coronary artery atherosclerosis in subordinate intact females may have been related in some way to chronic ovarian dysfunction observed in seven of 12 of these individuals. As a group, subordinate intact females also had enlarged adrenal glands, suggestive of mechanisms that may influence atherogenesis independently. The results indicate that, in this species, ovariectomy and chronic ovarian dysfunction related to subordinate social status are associated with a more atherogenic plasma lipid pattern and abolish "female protection" against coronary artery atherosclerosis.

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Section: Discussionmentioning

confidence: 96%

Ovariectomy, social status, and atherosclerosis in cynomolgus monkeys.

Adams¹,

Kaplan²,

Clarkson³

et al. 1985

Arteriosclerosis

151

View full text Add to dashboard Cite

show abstract

“…Previous observations have shown that cellular growth from the same tissue source can respond to estrogen in a diverse fashion. For example, vascular smooth muscle cells can be stimulated or growth-inhibited by estrogen (6,33,42,43,60). Similarly, breast cancer cell growth can be estrogen-dependent or estrogen-resistant.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, growth inhibition was observed in response to estrogen in vascular smooth muscle cells that normally express tuberin (33,(42)(43)(44). Thus, we examined the effect of tuberin expression on the growth of ELT-3 cells in response to estrogen.…”

Section: Tuberin Binds To Er␣ In Vivo and Modulates Growth Of Elt-3 Cmentioning

confidence: 99%

Estrogen-induced Smooth Muscle Cell Growth Is Regulated by Tuberin and Associated with Altered Activation of Platelet-derived Growth Factor Receptor-β and ERK-1/2

Finlay

York

Karas

et al. 2004

Journal of Biological Chemistry

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The mechanisms that regulate the diverse responses to estrogen (E 2 ) are unknown. Loss of function of the tuberous sclerosis 2 gene (TSC2), a tumor suppressor gene, has been associated with a growth-promoting effect of E 2 . We hypothesized that tuberin, the protein product of TSC2, binds to estrogen receptors (ER) and regulates the growth effect of E 2 . An in vivo association between full-length tuberin and ER␣ was observed in HEK 293 cells and ELT-3 smooth muscle cells. In contrast, poor association was observed between tuberin and ER␤. Complex formation with ER␣ and the C-terminal end of tuberin was also observed in vivo and in vitro, indicating that binding between ER␣ and tuberin occurs at the C-terminal end of the tuberin molecule. We examined the effect of tuberin expression in ELT-3 smooth

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“…However, systemic effects of estrogens do not account fo ~" the majority of the observed atheroprotective effects of E2 [2.3,15,16]. In an effort to reveal additional pathways that may mediate the atheroprotective effects of E2, direct effects of E2 ol ~, vascular cells are currently being investigated (reviewed in [1 '] Direct effects of E2 on vascular cell function were first suggested decades ago [7,18] and have since been shown both in whole animal and in vitro studies [10,[19][20][21][22][23][24][25][26][27][28][29][30]. However, the signaling pathways involved in the direct effects of E2 on vascular cells are not yet characterized.…”

Section: Introductionmentioning

confidence: 99%