17β-Estradiol modulates endothelin-1 expression and release in human endothelial cells

Bilsel, A Serpil; Moini, Hadi; Tetik, Erkan; Aksungar, Fehime Benli; Kaynak, Bogaç; Özer, Ayşe

doi:10.1016/s0008-6363(00)00046-8

Cited by 61 publications

(42 citation statements)

References 32 publications

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“…Such polar secretion occurs in endothelial cells (33), and is likely critical to the role of ET-1 as a paracrine/autocrine mediator. We found that AEC produce ET-1 at levels comparable to those of endothelial cells (34,35). In addition, AEC-associated ET-1 was detected predominantly in the cytoplasm by immunocytofluorescence, and some ET-1 immunoreactivity was also detected in the nucleus.…”

Section: Discussionmentioning

confidence: 62%

Endothelin-1 Induces Alveolar Epithelial–Mesenchymal Transition through Endothelin Type A Receptor–Mediated Production of TGF-β1

Jain

Shaul²,

Borok³

et al. 2007

Am J Respir Cell Mol Biol

140

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Endothelin-1 (ET-1) is implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF), but the cellular mechanisms underlying the role it plays in this disease are not well characterized. Epithelialmesenchymal transition (EMT), which was recently demonstrated in alveolar epithelial cells (AEC), may play an important role in the pathogenesis of IPF and other forms of pulmonary fibrosis. Whether ET-1 contributes to the induction of EMT in AEC is unknown. The aims of this study were to evaluate AEC production of ET-1 and to determine if ET-1 induces EMT in AEC. We demonstrate that ET-1 is produced at physiologically relevant levels by primary AEC and is secreted preferentially toward the basolateral surface. We also demonstrate that AEC express high levels of endothelin type A receptors (ET-A) and, to a lesser extent, type B receptors (ET-B), suggesting autocrine or paracrine function for alveolar ET-1. In addition, ET-1 induces EMT through ET-A activation. Furthermore, TGF-␤1 synthesis is increased by ET-1, ET-1 induces Smad3 phosphorylation, and ET-1-induced EMT is attenuated by a TGF-␤1-neutralizing antibody. Thus, ET-1 is an important mediator of EMT in AEC, acting through ET-A-mediated TGF-␤1 production. These findings increase our basic understanding of the role of ET-1 in pulmonary fibrosis and suggest potential roles for AEC-derived ET-1 in the pathogenesis of other alveolar epithelial-mediated lung diseases.

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Section: Discussionmentioning

confidence: 62%

Endothelin-1 Induces Alveolar Epithelial–Mesenchymal Transition through Endothelin Type A Receptor–Mediated Production of TGF-β1

Jain

Shaul²,

Borok³

et al. 2007

Am J Respir Cell Mol Biol

140

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“…Estrogen also inhibits the endothelin release from endothelial cells in bovine artery 75 and human umbilical vein 76 which may contribute to prevent circulatory failure. This is at least partly mediated by the inhibition of mitogen-activated protein kinase activity.…”

Section: Inhibition Of Vasoconstrictive Reactionmentioning

confidence: 99%

Which Gender is Better Positioned in the Process of Liver Surgery? Male or Female?

2007

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Liver surgery is a process which induces various types of stress on the liver including the total occlusion of the blood inflow, hemorrhage, massive volume reduction, and postoperative infection. Animal studies have shown a gender dimorphic response of the liver for various stresses such as ischemia/reperfusion, hemorrhage/resuscitation, hepatectomy, portal branch ligation, and endotoxemia. Most of these studies demonstrated the female liver to be more tolerant under stressful conditions than the male liver. Estrogen, which is a representative female sex hormone, may be one of the responsible factors for this gender dimorphism. The mechanism of estrogen's salutary effect includes circulatory improvement, a reduced inflammatory response, a reduced oxygen radical production, and an improved hepatic regeneration. However, the clinical evidence that supports the results of these experimental studies is still insufficient. A well-controlled prospective clinical study is necessary to clarify the role of gender or sex hormone in the process of liver surgery. This may not only lead to a deeper understanding of the liver pathophysiology, but also to the possibility of hepatoprotective therapy using sex hormone modulators. This review summarizes the current understanding of gender dimorphism in the tolerance of the liver to various hepatic stresses, which occur during the process of major liver surgery.

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“…Endothelial cells cover the lumen of blood vessels and play an essential role in the regulation of vessel homeostasis and of flow and blood pressure in the circulatory system [17,18]. The endothelium is a dynamic system that is able to respond to different physical and chemical conditions through the production of many vasoactive substances such as endothelins (ETs), prostaglandin and nitric oxide (NO).…”

Section: Introductionmentioning

confidence: 99%

Hydrostatic pressure and shear stress affect endothelin‐1 and nitric oxide release by endothelial cells in bioreactors

Vozzi

Bianchi

Ahluwalia

et al. 2013

Biotechnology Journal

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Abundant experimental evidence demonstrates that endothelial cells are sensitive to flow; however, the effect of fluid pressure or pressure gradients that are used to drive viscous flow is not well understood. There are two principal physical forces exerted on the blood vessel wall by the passage of intra-luminal blood: pressure and shear. To analyze the effects of pressure and shear independently, these two stresses were applied to cultured cells in two different types of bioreactors: a pressure-controlled bioreactor and a laminar flow bioreactor, in which controlled levels of pressure or shear stress, respectively, can be generated. Using these bioreactor systems, endothelin-1 (ET-1) and nitric oxide (NO) release from human umbilical vein endothelial cells were measured under various shear stress and pressure conditions. Compared to the controls, a decrease of ET-1 production by the cells cultured in both bioreactors was observed, whereas NO synthesis was up-regulated in cells under shear stress, but was not modulated by hydrostatic pressure. These results show that the two hemodynamic forces acting on blood vessels affect endothelial cell function in different ways, and that both should be considered when planning in vitro experiments in the presence of flow. Understanding the individual and synergic effects of the two forces could provide important insights into physiological and pathological processes involved in vascular remodeling and adaptation.

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17β-Estradiol modulates endothelin-1 expression and release in human endothelial cells

Cited by 61 publications

References 32 publications

Endothelin-1 Induces Alveolar Epithelial–Mesenchymal Transition through Endothelin Type A Receptor–Mediated Production of TGF-β1

Endothelin-1 Induces Alveolar Epithelial–Mesenchymal Transition through Endothelin Type A Receptor–Mediated Production of TGF-β1

Which Gender is Better Positioned in the Process of Liver Surgery? Male or Female?

Hydrostatic pressure and shear stress affect endothelin‐1 and nitric oxide release by endothelial cells in bioreactors

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