scholarly journals Endothelial to Mesenchymal Transition Contributes to Endothelial Dysfunction in Pulmonary Arterial Hypertension

2015 ◽  
Vol 185 (7) ◽  
pp. 1850-1858 ◽  
Author(s):  
Robert B. Good ◽  
Adrian J. Gilbane ◽  
Sarah L. Trinder ◽  
Christopher P. Denton ◽  
Gerry Coghlan ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Mesenchymal Transition ◽  
Pulmonary Arterial ◽  
Endothelial To Mesenchymal Transition

scholarly journals Galectin-3 Mediates Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension

2019 ◽  
Vol 10 (4) ◽  
pp. 731 ◽  
Author(s):  
Tangzhiming Li ◽  
Lihuang Zha ◽  
Hui Luo ◽  
Suqi Li ◽  
Lin Zhao ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Mesenchymal Transition ◽  
Galectin 3 ◽  
Pulmonary Arterial ◽  
Endothelial To Mesenchymal Transition

Baicalein attenuates monocrotaline-induced pulmonary arterial hypertension by inhibiting endothelial-to-mesenchymal transition

Life Sciences ◽  
2018 ◽  
Vol 207 ◽  
pp. 442-450 ◽  
Author(s):  
Ruizan Shi ◽  
Diying Zhu ◽  
Zehui Wei ◽  
Naijie Fu ◽  
Chang Wang ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Mesenchymal Transition ◽  
Pulmonary Arterial ◽  
Endothelial To Mesenchymal Transition

scholarly journals Endothelial dysfunction in pulmonary arterial hypertension: an evolving landscape (2017 Grover Conference Series)

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321775291 ◽  
Author(s):  
Benoît Ranchoux ◽  
Lloyd D. Harvey ◽  
Ramon J. Ayon ◽  
Aleksandra Babicheva ◽  
Sebastien Bonnet ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Molecular Mechanisms ◽  
Right Heart Failure ◽  
Vascular Pathology ◽  
Mesenchymal Transition ◽  
Conference Series ◽  
Major Player ◽  
Pulmonary Arterial

Endothelial dysfunction is a major player in the development and progression of vascular pathology in pulmonary arterial hypertension (PAH), a disease associated with small vessel loss and obstructive vasculopathy that leads to increased pulmonary vascular resistance, subsequent right heart failure, and premature death. Over the past ten years, there has been tremendous progress in our understanding of pulmonary endothelial biology as it pertains to the genetic and molecular mechanisms that orchestrate the endothelial response to direct or indirect injury, and how their dysregulation can contribute to the pathogenesis of PAH. As one of the major topics included in the 2017 Grover Conference Series, discussion centered on recent developments in four areas of pulmonary endothelial biology: (1) angiogenesis; (2) endothelial-mesenchymal transition (EndMT); (3) epigenetics; and (4) biology of voltage-gated ion channels. The present review will summarize the content of these discussions and provide a perspective on the most promising aspects of endothelial dysfunction that may be amenable for therapeutic development.

scholarly journals Paeoniflorin Ameliorates Chronic Hypoxia/SU5416-Induced Pulmonary Arterial Hypertension by Inhibiting Endothelial-to-Mesenchymal Transition

2020 ◽  
Vol Volume 14 ◽  
pp. 1191-1202 ◽  
Author(s):  
Min Yu ◽  
Liyao Peng ◽  
Ping Liu ◽  
Mingxia Yang ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Chronic Hypoxia ◽  
Mesenchymal Transition ◽  
Pulmonary Arterial ◽  
Endothelial To Mesenchymal Transition

scholarly journals Isolation and characterization of endothelial-to-mesenchymal transition cells in pulmonary arterial hypertension

2018 ◽  
Vol 314 (1) ◽  
pp. L118-L126 ◽  
Author(s):  
Toshio Suzuki ◽  
Erica J. Carrier ◽  
Megha H. Talati ◽  
Anandharajan Rathinasabapathy ◽  
Xinping Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Conditioned Medium ◽  
Mesenchymal Cells ◽  
Paracrine Effects ◽  
Mesenchymal Transition ◽  
Pulmonary Arterial ◽  
Endothelial To Mesenchymal Transition

Endothelial-to-mesenchymal transition (EndMT) is a process in which endothelial cells lose polarity and cell-to cell contacts, and undergo a dramatic remodeling of the cytoskeleton. It has been implicated in initiation and progression of pulmonary arterial hypertension (PAH). However, the characteristics of cells which have undergone EndMT cells in vivo have not been reported and so remain unclear. To study this, sugen5416 and hypoxia (SuHx)-induced PAH was established in Cdh5-Cre/Gt(ROSA)26Sortm4(ACTB-tdTomato,EGFP)Luo/J double transgenic mice, in which GFP was stably expressed in pan-endothelial cells. After 3 wk of SuHx, flow cytometry and immunohistochemistry demonstrated CD144-negative and GFP-positive cells (complete EndMT cells) possessed higher proliferative and migratory activity compared with other mesenchymal cells. While CD144-positive and α-smooth muscle actin (α-SMA)-positive cells (partial EndMT cells) continued to express endothelial progenitor cell markers, complete EndMT cells were Sca-1-rich mesenchymal cells with high proliferative and migratory ability. When transferred in fibronectin-coated chamber slides containing smooth muscle media, α-SMA robustly expressed in these cells compared with cEndMT cells that were grown in maintenance media. Demonstrating additional paracrine effects, conditioned medium from isolated complete EndMT cells induced enhanced mesenchymal proliferation and migration and increased angiogenesis compared with conditioned medium from resident mesenchymal cells. Overall, these findings show that EndMT cells could contribute to the pathogenesis of PAH both directly, by transformation into smooth muscle-like cells with higher proliferative and migratory potency, and indirectly, through paracrine effects on vascular intimal and medial proliferation.

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