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A20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF‐κB activation under hypoxia

A20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary arte... Full description

Journal Title: Journal of Cellular and Molecular Medicine July 2016, Vol.20(7), pp.1319-1328
Main Author: Li, Jing
Other Authors: Zhang, Linlin , Zhang, Yueming , Liu, Ying , Zhang, Hongyue , Wei, Liuping , Shen, Tingting , Jiang, Chun , Zhu, Daling
Format: Electronic Article Electronic Article
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Subjects:
A20
ID: ISSN: 1582-1838 ; E-ISSN: 1582-4934 ; DOI: 10.1111/jcmm.12816
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recordid: wj10.1111/jcmm.12816
title: A20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF‐κB activation under hypoxia
format: Article
creator:
  • Li, Jing
  • Zhang, Linlin
  • Zhang, Yueming
  • Liu, Ying
  • Zhang, Hongyue
  • Wei, Liuping
  • Shen, Tingting
  • Jiang, Chun
  • Zhu, Daling
subjects:
  • A20
  • Hypoxia
  • Angiogenesis
  • Pulmonary Artery Endothelial Cells
  • Nuclear Factor‐Kappa B
ispartof: Journal of Cellular and Molecular Medicine, July 2016, Vol.20(7), pp.1319-1328
description: A20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary artery endothelial cells (s). Here, we found a transient elevation of A20 expression in the lung tissues from hypoxic rats compared with normoxic controls. This rapid enhancement was mainly detected in the endothelium, and similar results were reproduced . During early hypoxia, genetic inhibition of A20 increased proliferation in pulmonary artery s, linking to advanced cell cycle progression as well as microtubule polymerization, and aggravated angiogenic effects including tube formation, cell migration and adhesion molecules expression. In addition, a negative feedback loop between nuclear factor‐kappa B and A20 was confirmed. Our findings provide evidence for an adaptive role of A20 against pulmonary artery s angiogenesis nuclear factor‐kappa B activation.
language:
source:
identifier: ISSN: 1582-1838 ; E-ISSN: 1582-4934 ; DOI: 10.1111/jcmm.12816
fulltext: fulltext
issn:
  • 1582-1838
  • 15821838
  • 1582-4934
  • 15824934
url: Link


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titleA20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF‐κB activation under hypoxia
creatorLi, Jing ; Zhang, Linlin ; Zhang, Yueming ; Liu, Ying ; Zhang, Hongyue ; Wei, Liuping ; Shen, Tingting ; Jiang, Chun ; Zhu, Daling
ispartofJournal of Cellular and Molecular Medicine, July 2016, Vol.20(7), pp.1319-1328
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subjectA20 ; Hypoxia ; Angiogenesis ; Pulmonary Artery Endothelial Cells ; Nuclear Factor‐Kappa B
descriptionA20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary artery endothelial cells (s). Here, we found a transient elevation of A20 expression in the lung tissues from hypoxic rats compared with normoxic controls. This rapid enhancement was mainly detected in the endothelium, and similar results were reproduced . During early hypoxia, genetic inhibition of A20 increased proliferation in pulmonary artery s, linking to advanced cell cycle progression as well as microtubule polymerization, and aggravated angiogenic effects including tube formation, cell migration and adhesion molecules expression. In addition, a negative feedback loop between nuclear factor‐kappa B and A20 was confirmed. Our findings provide evidence for an adaptive role of A20 against pulmonary artery s angiogenesis nuclear factor‐kappa B activation.
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titleA20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF‐κB activation under hypoxia
descriptionA20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary artery endothelial cells (s). Here, we found a transient elevation of A20 expression in the lung tissues from hypoxic rats compared with normoxic controls. This rapid enhancement was mainly detected in the endothelium, and similar results were reproduced . During early hypoxia, genetic inhibition of A20 increased proliferation in pulmonary artery s, linking to advanced cell cycle progression as well as microtubule polymerization, and aggravated angiogenic effects including tube formation, cell migration and adhesion molecules expression. In addition, a negative feedback loop between nuclear factor‐kappa B and A20 was confirmed. Our findings provide evidence for an adaptive role of A20 against pulmonary artery s angiogenesis nuclear factor‐kappa B activation.
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titleA20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF‐κB activation under hypoxia
authorLi, Jing ; Zhang, Linlin ; Zhang, Yueming ; Liu, Ying ; Zhang, Hongyue ; Wei, Liuping ; Shen, Tingting ; Jiang, Chun ; Zhu, Daling
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abstractA20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary artery endothelial cells (s). Here, we found a transient elevation of A20 expression in the lung tissues from hypoxic rats compared with normoxic controls. This rapid enhancement was mainly detected in the endothelium, and similar results were reproduced . During early hypoxia, genetic inhibition of A20 increased proliferation in pulmonary artery s, linking to advanced cell cycle progression as well as microtubule polymerization, and aggravated angiogenic effects including tube formation, cell migration and adhesion molecules expression. In addition, a negative feedback loop between nuclear factor‐kappa B and A20 was confirmed. Our findings provide evidence for an adaptive role of A20 against pulmonary artery s angiogenesis nuclear factor‐kappa B activation.
doi10.1111/jcmm.12816
pages1319-1328
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