17β-estradiol inhibits apoptosis of endothelial cells

Rene J. Alvarez, Sanford J. Gips, Nicanor Moldovan, Calvin C. Wilhide, Emily E. Milliken, Arthur T. Hoang, Ralph H. Hruban, Howard S. Silverman, Chi V. Dang, Pascal Goldschmidt-Clermont

Research output: Contribution to journalArticle

104 Citations (Scopus)

Abstract

Endothelial cells provide an antithrombotic and antiinflammatory barrier for the normal vessel wall. Dysfunction of endothelial cells has been shown to promote atherosclerosis, and normalization of previously dysfunctional endothelial cells can inhibit the genesis of atheroma. In normal arteries, endothelial cells are remarkably quiescent. Acceleration of the turnover rate of endothelial cells can lead to their dysfunction. Apoptosis is a physiological process that contributes to vessel homeostasis, by eliminating damaged cells from the vessel wall. However, increased endothelial cell turnover mediated through accelerated apoptosis may alter the function of the endothelium and therefore, promote atherosclerosis. Apoptotic endothelial cells can be detected on the luminal surface of atherosclerotic coronary vessels, but not in normal vessels. This finding links endothelial cell apoptosis and the process of atherosclerosis, although a causative role for apoptosis in this process remains hypothetical. Estrogen metabolites have been shown to be among the most potent anti-atherogenic agents available to date for post-menopausal women. The mechanism of estrogen's protective effect is currently incompletely characterized. Here we show that 17β-estradiol, a key estrogen metabolite, inhibits apoptosis in cultured endothelial cells. Our data support the hypothesis that 17β-estradiol's anti-apoptotic effect may be mediated via improved endothelial cell interaction with the substratum, increased tyrosine phosphorylation of pp125 focal adhesion kinase, and a subsequent reduction in programmed cell death of endothelial cells. Inhibition of apoptosis by estrogens may account for some of the anti-atherogenic properties of these compounds.

Original languageEnglish
Pages (from-to)372-381
Number of pages10
JournalBiochemical and Biophysical Research Communications
Volume237
Issue number2
DOIs
StatePublished - Aug 18 1997
Externally publishedYes

Fingerprint

Endothelial cells
Estradiol
Endothelial Cells
Apoptosis
Estrogens
Atherosclerosis
Metabolites
Physiological Phenomena
Focal Adhesion Protein-Tyrosine Kinases
Phosphorylation
Cell death
Atherosclerotic Plaques
Cell Communication
Cell Wall
Endothelium
Tyrosine
Cultured Cells
Coronary Vessels
Homeostasis
Cell Death

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Alvarez, R. J., Gips, S. J., Moldovan, N., Wilhide, C. C., Milliken, E. E., Hoang, A. T., ... Goldschmidt-Clermont, P. (1997). 17β-estradiol inhibits apoptosis of endothelial cells. Biochemical and Biophysical Research Communications, 237(2), 372-381. https://doi.org/10.1006/bbrc.1997.7085

17β-estradiol inhibits apoptosis of endothelial cells. / Alvarez, Rene J.; Gips, Sanford J.; Moldovan, Nicanor; Wilhide, Calvin C.; Milliken, Emily E.; Hoang, Arthur T.; Hruban, Ralph H.; Silverman, Howard S.; Dang, Chi V.; Goldschmidt-Clermont, Pascal.

In: Biochemical and Biophysical Research Communications, Vol. 237, No. 2, 18.08.1997, p. 372-381.

Research output: Contribution to journalArticle

Alvarez, RJ, Gips, SJ, Moldovan, N, Wilhide, CC, Milliken, EE, Hoang, AT, Hruban, RH, Silverman, HS, Dang, CV & Goldschmidt-Clermont, P 1997, '17β-estradiol inhibits apoptosis of endothelial cells', Biochemical and Biophysical Research Communications, vol. 237, no. 2, pp. 372-381. https://doi.org/10.1006/bbrc.1997.7085
Alvarez RJ, Gips SJ, Moldovan N, Wilhide CC, Milliken EE, Hoang AT et al. 17β-estradiol inhibits apoptosis of endothelial cells. Biochemical and Biophysical Research Communications. 1997 Aug 18;237(2):372-381. https://doi.org/10.1006/bbrc.1997.7085
Alvarez, Rene J. ; Gips, Sanford J. ; Moldovan, Nicanor ; Wilhide, Calvin C. ; Milliken, Emily E. ; Hoang, Arthur T. ; Hruban, Ralph H. ; Silverman, Howard S. ; Dang, Chi V. ; Goldschmidt-Clermont, Pascal. / 17β-estradiol inhibits apoptosis of endothelial cells. In: Biochemical and Biophysical Research Communications. 1997 ; Vol. 237, No. 2. pp. 372-381.
@article{318913fbdb8c4f19b8fe7f36c4745acd,
title = "17β-estradiol inhibits apoptosis of endothelial cells",
abstract = "Endothelial cells provide an antithrombotic and antiinflammatory barrier for the normal vessel wall. Dysfunction of endothelial cells has been shown to promote atherosclerosis, and normalization of previously dysfunctional endothelial cells can inhibit the genesis of atheroma. In normal arteries, endothelial cells are remarkably quiescent. Acceleration of the turnover rate of endothelial cells can lead to their dysfunction. Apoptosis is a physiological process that contributes to vessel homeostasis, by eliminating damaged cells from the vessel wall. However, increased endothelial cell turnover mediated through accelerated apoptosis may alter the function of the endothelium and therefore, promote atherosclerosis. Apoptotic endothelial cells can be detected on the luminal surface of atherosclerotic coronary vessels, but not in normal vessels. This finding links endothelial cell apoptosis and the process of atherosclerosis, although a causative role for apoptosis in this process remains hypothetical. Estrogen metabolites have been shown to be among the most potent anti-atherogenic agents available to date for post-menopausal women. The mechanism of estrogen's protective effect is currently incompletely characterized. Here we show that 17β-estradiol, a key estrogen metabolite, inhibits apoptosis in cultured endothelial cells. Our data support the hypothesis that 17β-estradiol's anti-apoptotic effect may be mediated via improved endothelial cell interaction with the substratum, increased tyrosine phosphorylation of pp125 focal adhesion kinase, and a subsequent reduction in programmed cell death of endothelial cells. Inhibition of apoptosis by estrogens may account for some of the anti-atherogenic properties of these compounds.",
author = "Alvarez, {Rene J.} and Gips, {Sanford J.} and Nicanor Moldovan and Wilhide, {Calvin C.} and Milliken, {Emily E.} and Hoang, {Arthur T.} and Hruban, {Ralph H.} and Silverman, {Howard S.} and Dang, {Chi V.} and Pascal Goldschmidt-Clermont",
year = "1997",
month = "8",
day = "18",
doi = "10.1006/bbrc.1997.7085",
language = "English",
volume = "237",
pages = "372--381",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - 17β-estradiol inhibits apoptosis of endothelial cells

AU - Alvarez, Rene J.

AU - Gips, Sanford J.

AU - Moldovan, Nicanor

AU - Wilhide, Calvin C.

AU - Milliken, Emily E.

AU - Hoang, Arthur T.

AU - Hruban, Ralph H.

AU - Silverman, Howard S.

AU - Dang, Chi V.

AU - Goldschmidt-Clermont, Pascal

PY - 1997/8/18

Y1 - 1997/8/18

N2 - Endothelial cells provide an antithrombotic and antiinflammatory barrier for the normal vessel wall. Dysfunction of endothelial cells has been shown to promote atherosclerosis, and normalization of previously dysfunctional endothelial cells can inhibit the genesis of atheroma. In normal arteries, endothelial cells are remarkably quiescent. Acceleration of the turnover rate of endothelial cells can lead to their dysfunction. Apoptosis is a physiological process that contributes to vessel homeostasis, by eliminating damaged cells from the vessel wall. However, increased endothelial cell turnover mediated through accelerated apoptosis may alter the function of the endothelium and therefore, promote atherosclerosis. Apoptotic endothelial cells can be detected on the luminal surface of atherosclerotic coronary vessels, but not in normal vessels. This finding links endothelial cell apoptosis and the process of atherosclerosis, although a causative role for apoptosis in this process remains hypothetical. Estrogen metabolites have been shown to be among the most potent anti-atherogenic agents available to date for post-menopausal women. The mechanism of estrogen's protective effect is currently incompletely characterized. Here we show that 17β-estradiol, a key estrogen metabolite, inhibits apoptosis in cultured endothelial cells. Our data support the hypothesis that 17β-estradiol's anti-apoptotic effect may be mediated via improved endothelial cell interaction with the substratum, increased tyrosine phosphorylation of pp125 focal adhesion kinase, and a subsequent reduction in programmed cell death of endothelial cells. Inhibition of apoptosis by estrogens may account for some of the anti-atherogenic properties of these compounds.

AB - Endothelial cells provide an antithrombotic and antiinflammatory barrier for the normal vessel wall. Dysfunction of endothelial cells has been shown to promote atherosclerosis, and normalization of previously dysfunctional endothelial cells can inhibit the genesis of atheroma. In normal arteries, endothelial cells are remarkably quiescent. Acceleration of the turnover rate of endothelial cells can lead to their dysfunction. Apoptosis is a physiological process that contributes to vessel homeostasis, by eliminating damaged cells from the vessel wall. However, increased endothelial cell turnover mediated through accelerated apoptosis may alter the function of the endothelium and therefore, promote atherosclerosis. Apoptotic endothelial cells can be detected on the luminal surface of atherosclerotic coronary vessels, but not in normal vessels. This finding links endothelial cell apoptosis and the process of atherosclerosis, although a causative role for apoptosis in this process remains hypothetical. Estrogen metabolites have been shown to be among the most potent anti-atherogenic agents available to date for post-menopausal women. The mechanism of estrogen's protective effect is currently incompletely characterized. Here we show that 17β-estradiol, a key estrogen metabolite, inhibits apoptosis in cultured endothelial cells. Our data support the hypothesis that 17β-estradiol's anti-apoptotic effect may be mediated via improved endothelial cell interaction with the substratum, increased tyrosine phosphorylation of pp125 focal adhesion kinase, and a subsequent reduction in programmed cell death of endothelial cells. Inhibition of apoptosis by estrogens may account for some of the anti-atherogenic properties of these compounds.

UR - http://www.scopus.com/inward/record.url?scp=0031577348&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031577348&partnerID=8YFLogxK

U2 - 10.1006/bbrc.1997.7085

DO - 10.1006/bbrc.1997.7085

M3 - Article

C2 - 9268719

AN - SCOPUS:0031577348

VL - 237

SP - 372

EP - 381

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -