Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells

Vitronectin (VN) is a multi-functional protein involved in extracellular matrix (ECM)-cell binding through integrin receptors on the cell surface, which is an important environmental process for maintaining biological homeostasis. We investigated how VN affects the survival of endothelial cells afte...

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Main Authors: Hazawa, Masaharu, Yasuda, Takeshi, Noshiro, Katsuko, Saotome-Nakamura, Ai, Fukuzaki, Tomoko, Michikawa, Yuichi, Gotoh, Takaya, Tajima, Katsushi
Format: Online
Language:English
Published: Elsevier 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678119/
id pubmed-3678119
recordtype oai_dc
spelling pubmed-36781192013-06-14 Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells Hazawa, Masaharu Yasuda, Takeshi Noshiro, Katsuko Saotome-Nakamura, Ai Fukuzaki, Tomoko Michikawa, Yuichi Gotoh, Takaya Tajima, Katsushi Article Vitronectin (VN) is a multi-functional protein involved in extracellular matrix (ECM)-cell binding through integrin receptors on the cell surface, which is an important environmental process for maintaining biological homeostasis. We investigated how VN affects the survival of endothelial cells after radiation damage. VN attenuated radiation-induced expression of p21, an inhibitor of cell cycle progression, and selectively inhibited Erk- and p38 MAPK-dependent p21 induction after radiation exposure through regulation of the activity of GSK-3β. VN also reduced the cleavage of caspase-3, thereby inhibiting radiation-induced apoptotic cell death. These results suggest that VN has important roles in cell survival after radiation damage. Elsevier 2012-10-17 /pmc/articles/PMC3678119/ /pubmed/23772367 http://dx.doi.org/10.1016/j.fob.2012.10.002 Text en © 2012 Published by Elsevier B.V. on behalf of Federation of European Biochemical Societies. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non- commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Hazawa, Masaharu
Yasuda, Takeshi
Noshiro, Katsuko
Saotome-Nakamura, Ai
Fukuzaki, Tomoko
Michikawa, Yuichi
Gotoh, Takaya
Tajima, Katsushi
spellingShingle Hazawa, Masaharu
Yasuda, Takeshi
Noshiro, Katsuko
Saotome-Nakamura, Ai
Fukuzaki, Tomoko
Michikawa, Yuichi
Gotoh, Takaya
Tajima, Katsushi
Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
author_facet Hazawa, Masaharu
Yasuda, Takeshi
Noshiro, Katsuko
Saotome-Nakamura, Ai
Fukuzaki, Tomoko
Michikawa, Yuichi
Gotoh, Takaya
Tajima, Katsushi
author_sort Hazawa, Masaharu
title Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
title_short Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
title_full Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
title_fullStr Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
title_full_unstemmed Vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
title_sort vitronectin improves cell survival after radiation injury in human umbilical vein endothelial cells
description Vitronectin (VN) is a multi-functional protein involved in extracellular matrix (ECM)-cell binding through integrin receptors on the cell surface, which is an important environmental process for maintaining biological homeostasis. We investigated how VN affects the survival of endothelial cells after radiation damage. VN attenuated radiation-induced expression of p21, an inhibitor of cell cycle progression, and selectively inhibited Erk- and p38 MAPK-dependent p21 induction after radiation exposure through regulation of the activity of GSK-3β. VN also reduced the cleavage of caspase-3, thereby inhibiting radiation-induced apoptotic cell death. These results suggest that VN has important roles in cell survival after radiation damage.
publisher Elsevier
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678119/
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