Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head

Vascular injury is considered an important pathological process during glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH). In this study, we tried to investigate whether the endoplasmic reticulum (ER) stress is triggered in the GC-induced endotheliocyte (EC) apoptosis and ONFH. The...

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Autores principales: Gao, Yanchun, Zhu, Hongyi, Wang, Qiyang, Feng, Yong, Zhang, Changqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2020
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990927/
https://www.ncbi.nlm.nih.gov/pubmed/32025204
http://dx.doi.org/10.7150/ijbs.35256
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author Gao, Yanchun
Zhu, Hongyi
Wang, Qiyang
Feng, Yong
Zhang, Changqing
author_facet Gao, Yanchun
Zhu, Hongyi
Wang, Qiyang
Feng, Yong
Zhang, Changqing
author_sort Gao, Yanchun
collection PubMed
description Vascular injury is considered an important pathological process during glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH). In this study, we tried to investigate whether the endoplasmic reticulum (ER) stress is triggered in the GC-induced endotheliocyte (EC) apoptosis and ONFH. The results showed that a GC upregulated the expression of ER stress-related proteins, and PERK-CHOP signaling played an important role and induced EC apoptosis. The inhibition of PERK by GSK2656157 significantly decreased the GC-induced EC apoptosis in vitro and in vivo, thus protecting a rat model from vascular injury and significantly preventing GC-induced ONFH.
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spelling pubmed-69909272020-02-05 Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head Gao, Yanchun Zhu, Hongyi Wang, Qiyang Feng, Yong Zhang, Changqing Int J Biol Sci Research Paper Vascular injury is considered an important pathological process during glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH). In this study, we tried to investigate whether the endoplasmic reticulum (ER) stress is triggered in the GC-induced endotheliocyte (EC) apoptosis and ONFH. The results showed that a GC upregulated the expression of ER stress-related proteins, and PERK-CHOP signaling played an important role and induced EC apoptosis. The inhibition of PERK by GSK2656157 significantly decreased the GC-induced EC apoptosis in vitro and in vivo, thus protecting a rat model from vascular injury and significantly preventing GC-induced ONFH. Ivyspring International Publisher 2020-01-01 /pmc/articles/PMC6990927/ /pubmed/32025204 http://dx.doi.org/10.7150/ijbs.35256 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Gao, Yanchun
Zhu, Hongyi
Wang, Qiyang
Feng, Yong
Zhang, Changqing
Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title_full Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title_fullStr Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title_full_unstemmed Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title_short Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head
title_sort inhibition of perk signaling prevents against glucocorticoid-induced endotheliocyte apoptosis and osteonecrosis of the femoral head
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990927/
https://www.ncbi.nlm.nih.gov/pubmed/32025204
http://dx.doi.org/10.7150/ijbs.35256
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