scholarly journals The Impact of Estrogen Receptor in Arterial and Lymphatic Vascular Diseases

2020 ◽  
Vol 21 (9) ◽  
pp. 3244 ◽  
Author(s):  
Coralie Fontaine ◽  
Florent Morfoisse ◽  
Florence Tatin ◽  
Audrey Zamora ◽  
Rana Zahreddine ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Lymphatic Vessels ◽  
Vascular Diseases ◽  
Arterial Injury ◽  
Vascular Effects ◽  
Beneficial Effects ◽  
Estrogen Receptor Modulators ◽  
Lymphatic Diseases ◽  
Collateral Growth ◽  
The Impact

The lower incidence of cardiovascular diseases in pre-menopausal women compared to men is well-known documented. This protection has been largely attributed to the protective effect of estrogens, which exert many beneficial effects against arterial diseases, including vasodilatation, acceleration of healing in response to arterial injury, arterial collateral growth and atheroprotection. More recently, with the visualization of the lymphatic vessels, the impact of estrogens on lymphedema and lymphatic diseases started to be elucidated. These estrogenic effects are mediated not only by the classic nuclear/genomic actions via the specific estrogen receptor (ER) α and β, but also by rapid extra-nuclear membrane-initiated steroid signaling (MISS). The ERs are expressed by endothelial, lymphatic and smooth muscle cells in the different vessels. In this review, we will summarize the complex vascular effects of estrogens and selective estrogen receptor modulators (SERMs) that have been described using different transgenic mouse models with selective loss of ERα function and numerous animal models of vascular and lymphatic diseases.

scholarly journals Selective Estrogen Receptor Modulators Accelerate Cutaneous Wound Healing in Ovariectomized Female Mice

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 551-557 ◽  
Author(s):  
Matthew J. Hardman ◽  
Elaine Emmerson ◽  
Laura Campbell ◽  
Gillian S. Ashcroft
Keyword(s):  
Wound Healing ◽  
Estrogen Receptor ◽  
Selective Estrogen Receptor Modulators ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Beneficial Effects ◽  
Estrogen Receptor Modulators ◽  
Ovariectomized Mice ◽  
Receptor Modulators

A lack of systemic hormones in elderly postmenopausal women leads to delayed cutaneous wound healing. This effect can be reversed by systemic or topical estrogen replacement in both humans and rodent models. Over recent years selective estrogen receptor modulators have been developed in an attempt to achieve the beneficial effects of estrogen clinically, while minimizing the detrimental side effects. The effects of selective estrogen receptor modulators on the skin are poorly understood, and the effects on wound healing have not been assessed. In this study we treated 10-wk-old ovariectomized mice with estradiol, tamoxifen (TAM), raloxifene (RAL), or vehicle and examined the effect on healing of full-thickness incisional wounds. Both TAM and RAL substantially accelerate healing, associated with a dampened inflammatory response and altered inflammatory cytokine profile. In vitro TAM and RAL demonstrate antiinflammatory activity comparable to estrogen. These results have significant implications for the clinical modulation of wound healing.

scholarly journals Distinct Approaches of Raloxifene: Its Far-Reaching Beneficial Effects Implicating the HO-System

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Denise Börzsei ◽  
Renáta Szabó ◽  
Alexandra Hoffmann ◽  
Médea Veszelka ◽  
Imre Pávó ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Current Knowledge ◽  
Cardiovascular Effects ◽  
The Body ◽  
General Activity ◽  
Beneficial Effects ◽  
Cell Defense ◽  
Estrogen Receptor Modulators ◽  
Pathological Conditions ◽  
Receptor Modulators

Selective estrogen receptor modulators (SERMs) were discovered in the mid-1900s in connection with estrogen-related pathological conditions. They were developed to antagonize the adverse effects of estrogen and have been shown to be effective against postmenopausal disorders manifested by estrogen deficiency. Raloxifene (RAL), one of the most widely used SERMs, expresses estrogen-like effects on bones, while it is found to be an antagonist on breast and uterus. RAL has multiple beneficial effects throughout the body, including antioxidant and anti-inflammatory properties, because of which it gains particular attention. Additionally, previous studies have revealed that RAL is an efficient modulator of heme-oxygenase (HO) expression. HO, through its general activity, participates in comprehensive cell defense processes, thus the induction of HO by RAL administration indicates a major role in its therapeutic efficacy. In this review, we compile the current knowledge about the overall metabolic, neurocognitive, and cardiovascular effects of RAL involving the cytoprotective HO-system.

Inhibition of Leucocyte and Platelet Adhesion Reduces Neointimal Hyperplasia after Arterial Injury

1997 ◽  
Vol 77 (04) ◽  
pp. 783-788 ◽  
Author(s):  
Paolo Golino ◽  
Giuseppe Ambrosio ◽  
Massimo Ragni ◽  
Plinio Cirillo ◽  
Nicolino Esposito ◽  
...  
Keyword(s):  
Coronary Angioplasty ◽  
Neointimal Hyperplasia ◽  
Rabbit Model ◽  
Arterial Injury ◽  
Platelet Glycoprotein ◽  
Beneficial Effects ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Interaction ◽  
Adhesion Complex

SummaryRestenosis following coronary angioplasty is thought to result from migration and proliferation of medial smooth muscle cells. However, the factors that initiate this proliferation are still unknown. In a rabbit model of carotid artery injury, we tested the hypothesis that activated platelets and leucocytes might contribute to the development of neointimal hyperplasia. Following arterial injury, rabbits received either no treatment, R15.7, a monoclonal antibody against the leucocyte CD ll/CD 18 adhesion complex, aurintricarboxylic acid (ATA), a sub stance that inhibits platelet glycoprotein Ib-von Willebrand factor interaction, or the combination of R15.7 and ATA. After 21 days, the extent of neointimal hyperplasia was evaluated by planimetry on histological arterial sections. The area of neointima averaged 0.51 ±0.07 mm2 in control animals and it was significantly reduced by administrationof either R15.7 or ATA alone to 0.12 ± 0.05 and 0.20 ±0.01 mm2, respectively (p <0.05 vs controls for both groups). The animals that received the combination of R15.7 and ATA showed a further reduction in neointimal hyperplasia, as compared to animals that received ATA alone (p <0.05 vs ATA alone). These data indicate that platelets and leucocytes play animportant role in the pathophysi ology of neointimal hyperplasia in this experimental model. Interven tions that reduce platelet and leucocyte adhesion to vessel wall might have beneficial effects in reducing restenosis following coronary angioplasty.

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