Minimal effect of estrogens on endothelial cell growth and production of prostacyclin

Corvazier, Elisabeth; Dupuy, Évelyne; Dosne, A.M.; Maclouf, Jacques

doi:10.1016/0049-3848(84)90387-6

Cited by 22 publications

(9 citation statements)

References 21 publications

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“…Previous studies have shown that estrogen produces variable effects on endothelial cell growth (24). In HUVECs, estrogen has been reported to produce either stimulatory, inhibitory, or no effect on cell growth (6,31,32,44). The reason for this discrepancy is not known.…”

Section: Discussionmentioning

confidence: 89%

Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism

Cai

Yuan

Weng

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Growing evidences support that androgen displays beneficial effects on cardiovascular functions although the mechanism of androgen actions remains to be elucidated. Modulation of endothelial cell growth and function is a potential mechanism of androgen actions. We demonstrated in the present study that androgens [dihydrotestosterone (DHT) and testosterone], but not 17β-estradiol, produced a time- and dose-dependent induction of cell proliferation in primary human aortic endothelial cells (HAECs) as evident by increases in viable cell number and DNA biosynthesis. Real-time qRT-PCR analysis showed that DHT induced androgen receptor (AR), cyclin A, cyclin D1, and vascular endothelial growth factor (VEGF) gene expression in a dose- and time-dependent manner. The addition of casodex, a specific AR antagonist, or transfection of a specific AR siRNA blocked DHT-induced cell proliferation and target gene expression, indicating that the DHT effects are mediated via AR. Moreover, coadministration of SU5416 to block VEGF receptors, or transfection of a specific VEGF-A siRNA to knockdown VEGF expression, produced a dose-dependent blockade of DHT induction of cell proliferation and cyclin A gene expression. Interestingly, roscovitine, a selective cyclin-dependent kinase inhibitor, also blocked the DHT stimulation of cell proliferation with a selective inhibition of DHT-induced VEGF-A expression. These results indicate that androgens acting on AR stimulate cell proliferation through upregulation of VEGF-A, cyclin A, and cyclin D1 in HAECs, which may be beneficial to cardiovascular functions since endothelial cell proliferation could assist the repair of endothelial injury/damage in cardiovascular system.

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Section: Discussionmentioning

confidence: 89%

Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism

Cai

Yuan

Weng

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…Synthesis of the vasodilator prostacyclin and vasoconstrictor thromboxone (TXA 2 ), products of the COX (cyclooxygenase) pathway, may also be modulated by oestrogens. However, data on effects of oestrogens on prostanoid synthesis in cultured ECs are conflicting, with one report [52] showing an increase in prostacyclin production in response to E2, and another [53] showing no detectable changes in either basal or agonist-induced prostacyclin release. Interestingly, the rapid potentiation of acetylcholine-induced vasodilation in skin resistance arteries by E2 has been shown to be mediated via COX-2, one of the two isoforms of COX, a key enzyme in prostaglandin synthesis [54].…”

Section: Vascular Ecs (Endothelial Cells)mentioning

confidence: 92%

“…EC growth and death are important in vascular health and disease. In cell culture studies, oestrogen may promote growth of human ECs [29][30][31], although this finding is not universal [32][33][34]. E2 has been reported to inhibit EC apoptosis induced by the inflammatory factor TNF-α (tumour necrosis factor-α) [35,36] or hypoxia [37].…”

Section: Vascular Ecs (Endothelial Cells)mentioning

confidence: 96%

Cellular mechanisms underlying the cardiovascular actions of oestrogens

2006

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Although pre-menopausal women enjoy relative cardiovascular protection, hormone (oestrogen+/-progestin)-replacement therapy has not shown cardiovascular benefits in post-menopausal women, suggesting that the effects of oestrogens on the cardiovascular system are much more complex than previously expected. Endothelial cells, smooth muscle cells, cardiac myocytes and fibroblasts, the cellular components of blood vessels and the heart, play important roles in cardiovascular health and disease. During the development and progression of cardiovascular disease, changes occur both in the structure and function of these cells, resulting in a wide range of abnormalities, which affect growth, death and physiological function. These cells contain functional oestrogen receptors and are targets for oestrogen action. This review focuses on recent studies on the effects of oestrogen on cardiovascular cell function. Oestrogens, particularly 17beta-oestradiol, exert multiple effects on cardiovascular cells, and these effects may contribute to the gender-associated protection against cardiovascular diseases.

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“…This observation is consistent with the already established effect of estradiol per se in rodent and human endothelial cells. 11,18 To the extent that enhancement of endothelial cell replication retards vascular disease by promoting reendothelialization at areas of intimal microinjury in vivo, this effect of phytoestrogens 3 [H] thymidine incorporation in hormone-treated and control cells. * P Ͻ .05; ** P Ͻ .01; *** P Ͻ .001. may be beneficial for cardiovascular protection.…”

Section: Discussionmentioning

confidence: 99%

Effects of phytoestrogens on DNA synthesis and creatine kinase activity in vascular cells

Sömjen

Knoll

Kohen

et al. 2001

American Journal of Hypertension

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Minimal effect of estrogens on endothelial cell growth and production of prostacyclin

Cited by 22 publications

References 21 publications

Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism

Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism

Cellular mechanisms underlying the cardiovascular actions of oestrogens

Effects of phytoestrogens on DNA synthesis and creatine kinase activity in vascular cells

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