Effects of estradiol on myointimal thickenings from catheter injury and on organizing white mural non-occlusive thrombi

Weigensberg, Bernard I.; Lough, John; More, Robert H.; Katz, Emma; Pugash, E.; Peniston, Charles

doi:10.1016/0021-9150(84)90055-8

Cited by 26 publications

(5 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of observational epidemiological studies have demonstrated postmenopausal estrogen replacement therapy in women can decrease the incidence of myocardial infarction and cardiac death by 35-50% [2][3][4][5][6]. These epidemiologic studies are supported further by animal studies demonstrating E2-mediated inhibition of experimentally induced atherosclerosis [7][8][9][10][11][12]46]. The atheroprotectix e effects of E2 are generally believed to be mediated in part b3 effects of E2 on systemic factors such as serum lipid levels [2.13,14].…”

Section: Introductionmentioning

confidence: 99%

Human vascular smooth muscle cells express an estrogen receptor isoform

et al. 1995

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Human vascular smooth muscle cells express an estrogen receptor isoform

et al. 1995

View full text Add to dashboard Cite

“…[3][4][5][6][7][8] Estrogens are believed to exert direct anti-atherogenic effects through an initial interaction with the estrogen receptor (ER) in vascular smooth muscle cells (VSMCs). Furthermore, numerous clinical and epidemiological studies have demonstrated that the lack of estrogen is one of the risk factors for the development of atherosclerosis in postmenopausal women.…”

mentioning

confidence: 99%

“…2 In addition, results of several experimental studies have demonstrated that estrogen is predominantly involved in the developmental suppression of atherosclerosis in various animal models, suggesting that estrogens may have direct anti-atherogenic effects on the cardiovascular system of these animals. [3][4][5][6][7][8] Estrogens are believed to exert direct anti-atherogenic effects through an initial interaction with the estrogen receptor (ER) in vascular smooth muscle cells (VSMCs). Furthermore, numerous clinical and epidemiological studies have demonstrated that the lack of estrogen is one of the risk factors for the development of atherosclerosis in postmenopausal women.…”

mentioning

confidence: 99%

Steroid Sulfatase and Estrogen Sulfotransferase in the Atherosclerotic Human Aorta

Nakamura

Miki

Suzuki

et al. 2003

The American Journal of Pathology

View full text Add to dashboard Cite

Various epidemiological studies have demonstrated a relatively low incidence of cardiovascular events in premenopausal women and its marked increment after menopause. In addition, estrogens have been postulated to exert direct anti-atherogenic effects via binding to estrogen receptors in vascular smooth muscle cells (VSMCs). However, not all postmenopausal women develop atherosclerosis despite decreased levels of serum estrogen. Therefore, we believe it is important to examine the status of estrogen metabolism in situ in the human cardiovascular system. Estrone sulfate (E1S) is a major circulating plasma estrogen that is converted into the biologically active estrogen, estrone (E1) by steroid sulfatase (STS). E1 is also sulfated and reverted into E1S by estrogen sulfotransferase (EST). These two enzymes have recently been shown to play important roles in the in situ estrogen actions of estrogen-dependent human tissues and various sex steroid-dependent tumors. STS and EST, however, have not been studied in detail in the human vascular system associated with atherosclerotic changes. In the present study, we evaluated the relative abundance of STS-and ESTimmunoreactive protein and mRNA expression in human aorta using immunohistochemistry and reverse transcription followed by quantitative polymerase chain reaction in addition to enzyme activity. STS expression levels were found to be significantly higher in the VSMCs obtained from female aortas with mild atherosclerotic changes than in those with severe atherosclerotic changes and in male aortas regardless of atherosclerotic changes. EST expression levels in the VSMCs of these aortas, however, were significantly higher in female aortas with severe atherosclerotic changes and in male aortas than in female aortas with mild atherosclerotic changes. We believe it is important to examine factors regulating the expression and activity of these estrogen-metabolizing enzymes in the human aorta. Various cytokines have been proposed to function as regulators of these enzymes in other tissues. In the present study, we studied the effects of interleukin (IL)-1␤, known to be produced in human atherosclerotic lesions, on the expression of these enzymes using cultured human VSMCs originally obtained from a female patient. IL-1␤ markedly inhibited the expression of STS mRNA and enzyme activity, but stimulated the expression of EST mRNA and enzyme activity. In addition, IL-1␤ also reduced E2 production from E1S and E1 in VSMCs.Results from the present study seem to suggest that the expression levels of both STS and EST mRNA and activity may be significantly associated with the degree of atherosclerotic changes in the female aorta, which may be related to cytokines produced in situ, such as IL-1␤, in human atherosclerotic lesions. Various epidemiological studies have reported a relatively low incidence of cardiovascular events in premenopausal women and its marked increment after menopause.1 Estrogen has, therefore, been proposed as a cardioprotective agent, especially in women.2 In ...

show abstract

“…Thus it is possible that acute (within 60 min) administration could increase vasodilation in premenopausal women. However, evidence suggests that blood vessel integrity is well protected in premenopausal women, and estrogen may 1) inhibit the release of a vasoconstrictor substance such as endothelin (25), 2) decrease lipoprotein-induced smooth-muscle proliferation (7) in blood vessels, and 3) inhibit intimal proliferation associated with mechanical injury to endothelium (31,32,42). Thus relatively longer term ES had no effect on FBF in our subjects.…”

Section: Discussionmentioning

confidence: 77%

Effect of estrogen supplementation on exercise thermoregulation in premenopausal women

Chang¹,

Lambert²,

Moseley

et al. 1998

Journal of Applied Physiology

View full text Add to dashboard Cite

This study examined the effects of 3 days of estrogen supplementation (ES) on thermoregulation during exercise in premenopausal (20-39 yr) adult women during the follicular phase of the menstrual cycle. Subjects (11 control, 10 experimental) performed upright cycle ergometer exercise at 60% of maximal O2 consumption in a neutral environment (25 degreesC, 30% relative humidity) for 20 min. Subjects were given placebo (P) or beta-estradiol (2 mg/tablet, 3 tablets/day for 3 days). All experiments were conducted between 6:30 and 9:00 AM after ingestion of the last tablet. Heart rate, forearm blood flow (FBF), mean skin temperature, esophageal temperature (Tes), and forearm sweat rate were measured. Blood analysis for estrogen and progesterone reflected the follicular phase of the menstrual cycle. Maximal O2 consumption (37.1 +/- 6.2 in P vs. 38.4 +/- 6.3 ml. kg-1. min-1 in ES) and body weight-to-surface area ratio (35.58 +/- 2.85 in P vs. 37.3 +/- 2.7 in ES) were similar between groups. Synthesis of 70-kDa heat shock protein was not induced by 3 days of ES. Neither the threshold for sweating (36.97 +/- 0.15 in P vs. 36.90 +/- 0.22 degreesC in ES), the threshold for an increase in FBF (37.09 +/- 0. 22 in P vs. 37.17 +/- 0.26 degreesC in ES), the slope of sweat rate-Tes relationship (0.42 +/- 0.16 in P vs. 0.41 +/- 0.17 in ES), nor the FBF-Tes relationship (10.04 +/- 4.4 in P vs. 9.61 +/- 3.46 in ES) was affected (P > 0.05) by 3 days of ES. We conclude that 3 days of ES by young adult women in the follicular phase of their menstrual cycle have no effect on heat transfer to the skin, heat dissipation by evaporative cooling, or leukocyte synthesis of 70-kDa heat shock protein.

show abstract

Effects of estradiol on myointimal thickenings from catheter injury and on organizing white mural non-occlusive thrombi

Cited by 26 publications

References 14 publications

Human vascular smooth muscle cells express an estrogen receptor isoform

Human vascular smooth muscle cells express an estrogen receptor isoform

Steroid Sulfatase and Estrogen Sulfotransferase in the Atherosclerotic Human Aorta

Effect of estrogen supplementation on exercise thermoregulation in premenopausal women

Contact Info

Product

Resources

About