Oestradiol inhibits smooth muscle cell proliferation of pig coronary artery

Abstract

1 The effect of oestradiol 17p on vascular smooth muscle proliferation was examined in segments of the pig left anterior descending coronary artery (LAD). It was established by cytochemical techniques that out-growth from the segments was composed of vascular smooth muscle cells. 2 [3H]-thymidine uptake by pig LAD segments was used as an index of vascular smooth muscle cell proliferation. Nitroprusside and forskolin significantly inhibited [3H]-thymidine uptake and were used as positive controls. 3 Oestradiol 171 (180 -360 nM) inhibited thymidine uptake by pig LAD segments (P <0.05). The inhibition was observed only in the absence of phenol red, which is a weak oestrogen receptor agonist. The anti-oestrogens tamoxifen and its more potent metabolite 4-hydroxytamoxifen, both of which are partial oestrogen receptor agonists, also significantly inhibited thymidine uptake. However, pretreatment with either tamoxifen or 4-hydroxytamoxifen did not signficantly block oestradiol 17p-induced inhibition of thymidine uptake. 5 The data suggest that oestradiol 171 inhibits smooth muscle cell proliferation in porcine LAD segments, possibly through an oestrogen receptor mechanism. This in vitro effect suggests an in vivo role for oestradiol 171 in directly protecting coronary arteries against myointimal proliferation in premenopausal women.

Bisphenol A inhibits penile erection via alteration of histology in the rabbit

“…It has been well demonstrated that 17b-estradiol exhibits hypertrophy of uterine smooth muscle 19 but inhibits smooth muscle cell proliferation in porcine coronary. 20 Fotsis et al reported that the endogenous estrogen metabolite 2-methoxyestradiol inhibits angiogenesis in vitro. 21 In castrated or estrogen-treated animals, Data are expressed as mean AE standard deviation.…”

Estrogen inhibits the response-to-injury in a mouse carotid artery model.

“…Based on current models of atherosclerosis and restenosis after vascular injury (41,42), the known effects of estrogen, and the data presented here, a number of mechanisms might contribute to the estrogen effects on the response-to-injury observed in the present study. These potential mechanisms include (a) direct effects of estrogen on vascular smooth muscle cell proliferation (suggested previously in cell culture [23,24] and animal studies [9,[18][19][20][21][22] ); (b) inhibition of the synthesis and/or deposition of vascular matrix elements that contribute to lesion growth in injured vessels (43-45); (c) an altered rate of re-endothelialization after injury (17); and (d) estrogen inhibition of the inflammatory response in the injured vessel wall (46). This study was undertaken in C57BL/6J mice in part so that the mechanism of any effect noted might be studied next in C57BL/6J transgenic mice lacking the estrogen receptor (25,47).…”

“…In cultured vascular cells and tissue, 17,3-estradiol (E2)' also has been reported to inhibit the growth of vascular smooth muscle cells derived from rabbit aorta (23), and porcine coronary artery (24). However, interpretation of the effects of estrogen on atherogenesis and vascular cell growth in previous studies is complicated by the use of supraphysiologic (micromolar) estrogen dosing, atherogenic (high cholesterol) diets, and/or the absence of measured levels of circulating hormone.…”

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

“…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.…”