Effects of estradiol on platelet aggregation in mouse mesenteric arterioles and ex vivo

Rosenblum, William I.; El‐Sabban, Farouk; Allen, Alfred D.; Nelson, Guy H.; Bhatnagar, Ajay S.; Choi, Sung C.

doi:10.1016/0049-3848(85)90220-8

Cited by 14 publications

(5 citation statements)

References 22 publications

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“…A study published in 1985 has shown that mice treated by an estrogen pellet containing 0.5 mg of E2 and then submitted to a mesenteric endothelial injury exhibited a faster thrombosis response compared to the placebo group [33]. Similar results were found after a cerebral vessels injury induced by a noxious light/dye stimulus [34].…”

Section: Effects Of Estrogen Treatment On Platelet Activationmentioning

confidence: 71%

Effects of Estrogens on Platelets and Megakaryocytes

Dupuis

Séverin

Noirrit‐Esclassan

et al. 2019

IJMS

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In women, oral menopausal hormonal therapy (MHT) is associated with adverse effects including an increased incidence of thromboembolic events, classically attributed to an increase in several liver-derived coagulation factors due to hepatic first pass. While platelets are central players in thrombus constitution, their implication in women treated with estrogens remains incompletely characterized. Platelets and their medullar progenitors, megakaryocytes, express estrogen receptors (ER) that may explain, at least in part, a sensitivity to hormonal changes. The purpose of this review is to summarize our current knowledge of estrogen actions on platelets and megakaryocytes in mice following in vivo administration and in women using MHT.

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Section: Effects Of Estrogen Treatment On Platelet Activationmentioning

confidence: 71%

Effects of Estrogens on Platelets and Megakaryocytes

Dupuis

Séverin

Noirrit‐Esclassan

et al. 2019

IJMS

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“…Female C57Bl/6 mice were divided into five groups (n ϭ 5-13 per group) that received 17␤-estradiol alone (0.5 mg/pellet) or with tamoxifen (5 mg/pellet), tamoxifen alone (5 mg/pellet), 17␣-estradiol (0.5 mg/pellet), or placebo via 21-day release pellets implanted subcutaneously (IRA, Sarasota, Florida). The dose of 17␤-estradiol used in this study markedly elevates the plasma hormone level in mice (ϳ1,000 pg/ml) by 7 days after implantation, and these levels remain constant for 4 wk (49,50).…”

Section: Dnb Colitismentioning

confidence: 99%

Modulatory effects of estrogen in two murine models of experimental colitis

Verdú

Deng

Berčík

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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The association between oral contraceptives or pregnancy and inflammatory bowel disease is unclear. We investigated whether 17β-estradiol modulates intestinal inflammation in two models of colitis. Female mice were treated with 17β-estradiol alone or with tamoxifen, tamoxifen alone, 17α-estradiol, or placebo. Dinitrobenzene sulfonic acid (DNB)- or dextran sodium sulfate (DSS)-induced colitis were assessed macroscopically, histologically, and by myeloperoxidase (MPO) activity. Malondialdehyde and mRNA levels of intercellular adhesion molecule-1 (ICAM-1), interferon-γ (IFN-γ), and interleukin-13 (IL-13) were determined. In DNB colitis, 17β-estradiol alone, but not 17β-estradiol plus tamoxifen, or 17α-estradiol reduced macroscopic and histological scores, MPO activity and malondialdehyde levels. 17β-Estradiol also decreased the expression of ICAM-1, IFN-γ, and IL-13 mRNA levels compared with placebo. In contrast, 17β-Estradiol increased the macroscopic and histological scores compared with placebo in mice with DSS colitis. These results demonstrate anti-inflammatory and proinflammatory effects of 17β-estradiol in two different models of experimental colitis. The net modulatory effect most likely reflects a combination of estrogen receptor-mediated effects and antioxidant activity and may explain, in part, conflicting results from clinical trials.

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“…As such, the initial release of 17 β-E2 following implantation could have contributed to the observed uterine, vaginal and pituitary hyperplasia. Additionally, the few studies using mice that have measured 17 β-E2 concentrations as an end parameter have reported abnormal pharmacological responses (49) or strikingly high 17 β-E2 concentrations (53,54), even as long as 35 to 90 days after implantation of the pellets (55)(56)(57)(58).…”

Section: The Delivery Of Estrogens and Progesteronementioning

confidence: 99%

Estrogens and progesterone as neuroprotectants: what animal models teach us

Singh

Sumien²,

Kyser

et al. 2008

Front Biosci

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Estradiol and progesterone are two steroid hormones that target a variety of organ systems, including the heart, the bone and the brain. With respect to the latter, a large volume of basic science studies support the neuroprotective role of estradiol and/or progesterone. In fact, the results of such studies prompted the assessment of these hormones as protective agents against such disorders as Alzheimer's disease, stroke and traumatic brain injury. Interestingly, results from the Women's Health Initiative (WHI) yielded results that appeared to be inconsistent with the data derived from in vitro and in vivo models. However, we argue that the results from the basic science studies were not inconsistent with the clinical trials, but rather, are consistent with, and may even have predicted, the results from the WHI. To illustrate this point, we review here certain in vivo paradigms that have been used to assess the protective effects of estrogens and progesterone, and describe how the results from these animal models point to the importance of the type of hormone, the age of the subjects and the method of hormone administration, in determining whether or not hormones are neuroprotective. KeywordsEstrogens; Progestins; Neuroprotection; Alzheimer's disease; Animal Models; Review INTRODUCTIONThe U.S. Census Bureau estimates that by 2010, the population of women between 45 and 64 years old will reach approximately 42 million, a marked increase from the value reported for 2000 (approx. 32 million) (U.S. Census Bureau. Projected population of the United States, by Age and Sex: 200 to 2050. www.census.gov/ipc/www/usinterimproj/Internet release date: March 18, 2004). This increasing number of women will consequently need to make decisions about the use of hormone therapy to treat not only menopausal symptoms, but potentially, to maintain a healthy brain. And though numerous basic science studies, epidemiological studies and some clinical trials have supported the potential benefit of hormone therapy in reducing the incidence of age-associated brain dysfunction (including reducing the risk for Alzheimer's disease), recent results from the Women's Health Initiative (WHI) have suggested the contrary and left the field unsettled as to the future of hormone therapy. For example, caveats of the WHI (particularly the WHI memory study, WHIMS) include the possibility that both the age of the subjects and the duration of post-menopausal hormone deprivation diminish the protective brain response to steroid hormones. Additionally, the type of hormone (for example, While it is clear that a better understanding of the neurobiology of gonadal steroid hormones and their receptors is needed, it is equally important that we interpret the basic science studies appropriately, and understand their limitations if we are to apply the results from these studies towards the design of the next large-scale clinical trial or in fact, implement safer and more effective ways of treating the menopause and the post-menopausal period. To this end,...

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Effects of estradiol on platelet aggregation in mouse mesenteric arterioles and ex vivo

Cited by 14 publications

References 22 publications

Effects of Estrogens on Platelets and Megakaryocytes

Effects of Estrogens on Platelets and Megakaryocytes

Modulatory effects of estrogen in two murine models of experimental colitis

Estrogens and progesterone as neuroprotectants: what animal models teach us

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