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Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways

Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load signifi...

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Autores principales: Kong, Dechao, Zheng, Tiansheng, Zhang, Ming, Wang, Daode, Du, Shihao, Li, Xiang, Fang, Jiahu, Cao, Xiaojian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3716647/
https://www.ncbi.nlm.nih.gov/pubmed/23894471
http://dx.doi.org/10.1371/journal.pone.0069403
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author Kong, Dechao
Zheng, Tiansheng
Zhang, Ming
Wang, Daode
Du, Shihao
Li, Xiang
Fang, Jiahu
Cao, Xiaojian
author_facet Kong, Dechao
Zheng, Tiansheng
Zhang, Ming
Wang, Daode
Du, Shihao
Li, Xiang
Fang, Jiahu
Cao, Xiaojian
author_sort Kong, Dechao
collection PubMed
description Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load significantly reduced cell viability in a time- and load-dependent manner, as demonstrated by the Cell Counting Kit-8 (CCK-8) assay. Chondrocyte apoptosis induced by mechanical stress was confirmed by annexin V/propidium iodide (PI) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Western blot analysis revealed that static load-induced chondrocyte apoptosis was accompanied by increased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK). The loss of mitochondrial membrane potential (ΔΨm), increased Cytochrome c release, and activated Caspase-9 and Caspase-3, indicating that the mitochondrial pathway is involved in mechanical stress-induced chondrocyte apoptosis. Treatment with inhibitors of JNK (SP600125), p38 MAPK (SB203580), and ERK (PD98059) prior to mechanical stimulation reversed both the static load-induced chondrocyte apoptosis and the activation of JNK, p38 MAPK, and ERK. Taken together, the data presented in this study demonstrate that mechanical stress induces apoptosis in rat cervical endplate chondrocytes through the MAPK-mediated mitochondrial apoptotic pathway.
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spelling pubmed-37166472013-07-26 Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways Kong, Dechao Zheng, Tiansheng Zhang, Ming Wang, Daode Du, Shihao Li, Xiang Fang, Jiahu Cao, Xiaojian PLoS One Research Article Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load significantly reduced cell viability in a time- and load-dependent manner, as demonstrated by the Cell Counting Kit-8 (CCK-8) assay. Chondrocyte apoptosis induced by mechanical stress was confirmed by annexin V/propidium iodide (PI) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Western blot analysis revealed that static load-induced chondrocyte apoptosis was accompanied by increased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK). The loss of mitochondrial membrane potential (ΔΨm), increased Cytochrome c release, and activated Caspase-9 and Caspase-3, indicating that the mitochondrial pathway is involved in mechanical stress-induced chondrocyte apoptosis. Treatment with inhibitors of JNK (SP600125), p38 MAPK (SB203580), and ERK (PD98059) prior to mechanical stimulation reversed both the static load-induced chondrocyte apoptosis and the activation of JNK, p38 MAPK, and ERK. Taken together, the data presented in this study demonstrate that mechanical stress induces apoptosis in rat cervical endplate chondrocytes through the MAPK-mediated mitochondrial apoptotic pathway. Public Library of Science 2013-07-19 /pmc/articles/PMC3716647/ /pubmed/23894471 http://dx.doi.org/10.1371/journal.pone.0069403 Text en © 2013 Kong et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Kong, Dechao
Zheng, Tiansheng
Zhang, Ming
Wang, Daode
Du, Shihao
Li, Xiang
Fang, Jiahu
Cao, Xiaojian
Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title_full Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title_fullStr Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title_full_unstemmed Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title_short Static Mechanical Stress Induces Apoptosis in Rat Endplate Chondrocytes through MAPK and Mitochondria-Dependent Caspase Activation Signaling Pathways
title_sort static mechanical stress induces apoptosis in rat endplate chondrocytes through mapk and mitochondria-dependent caspase activation signaling pathways
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3716647/
https://www.ncbi.nlm.nih.gov/pubmed/23894471
http://dx.doi.org/10.1371/journal.pone.0069403
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