Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation

Detalhes bibliográficos
Autor(a) principal: Wang,Dong-Xiao
Data de Publicação: 2020
Outros Autores: Huang,Zheng, Li,Qing-Jie, Zhong,Guo-Qiang, He,Yan, Huang,Wei-Qiang, Cao,Xiao-Li, Tu,Rong-Hui, Meng,Jian-Jun
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Acta Cirúrgica Brasileira (Online)
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100201
Resumo: Abstract Purpose To investigate whether heat shock protein 90 (HSP90) is involved in complement regulation in ischemic postconditioning (IPC). Methods The left coronary artery of rats underwent 30 min of occlusion, followed by 120 min of reperfusion and treatment with IPC via 3 cycles of 30s reperfusion and 30s occlusion. The rats were injected intraperitoneally with 1 mg/kg HSP90 inhibitor geldanamycin (GA) after anesthesia. Eighty rats were randomly divided into four groups: sham, ischemia-reperfusion (I/R), IPC and IPC + GA. Myocardial infarct size, apoptosis index and the expression of HSP90, C3, C5a, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1β and c-Jun N-terminal kinase (JNK) were assessed. Results Compared with the I/R injury, the IPC treatment significantly reduced infarct size, release of troponin T, creatine kinase-MB, and lactate dehydrogenase, and cardiomyocyte apoptosis. These beneficial effects were accompanied by a decrease in TNF-α, IL-1β, C3, C5a and JNK expression levels. However, all these effects were abrogated by administration of the HSP90 inhibitor GA. Conclusion HSP90 exerts a profound effect on IPC cardioprotection, and may be linked to the inhibition of the complement system and JNK, ultimately attenuating I/R-induced myocardial injury and apoptosis.
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spelling Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammationHSP90 Heat-Shock ProteinsIschemic PostconditioningMAP Kinase Kinase 4InflammationRatsAbstract Purpose To investigate whether heat shock protein 90 (HSP90) is involved in complement regulation in ischemic postconditioning (IPC). Methods The left coronary artery of rats underwent 30 min of occlusion, followed by 120 min of reperfusion and treatment with IPC via 3 cycles of 30s reperfusion and 30s occlusion. The rats were injected intraperitoneally with 1 mg/kg HSP90 inhibitor geldanamycin (GA) after anesthesia. Eighty rats were randomly divided into four groups: sham, ischemia-reperfusion (I/R), IPC and IPC + GA. Myocardial infarct size, apoptosis index and the expression of HSP90, C3, C5a, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1β and c-Jun N-terminal kinase (JNK) were assessed. Results Compared with the I/R injury, the IPC treatment significantly reduced infarct size, release of troponin T, creatine kinase-MB, and lactate dehydrogenase, and cardiomyocyte apoptosis. These beneficial effects were accompanied by a decrease in TNF-α, IL-1β, C3, C5a and JNK expression levels. However, all these effects were abrogated by administration of the HSP90 inhibitor GA. Conclusion HSP90 exerts a profound effect on IPC cardioprotection, and may be linked to the inhibition of the complement system and JNK, ultimately attenuating I/R-induced myocardial injury and apoptosis.Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia2020-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100201Acta Cirúrgica Brasileira v.35 n.1 2020reponame:Acta Cirúrgica Brasileira (Online)instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)instacron:SBDPC10.1590/s0102-865020200010000005info:eu-repo/semantics/openAccessWang,Dong-XiaoHuang,ZhengLi,Qing-JieZhong,Guo-QiangHe,YanHuang,Wei-QiangCao,Xiao-LiTu,Rong-HuiMeng,Jian-Juneng2020-03-16T00:00:00Zoai:scielo:S0102-86502020000100201Revistahttps://www.bvs-vet.org.br/vetindex/periodicos/acta-cirurgica-brasileira/https://old.scielo.br/oai/scielo-oai.php||sgolden@terra.com.br0102-86501678-2674opendoar:2020-03-16T00:00Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)false
dc.title.none.fl_str_mv Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
title Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
spellingShingle Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
Wang,Dong-Xiao
HSP90 Heat-Shock Proteins
Ischemic Postconditioning
MAP Kinase Kinase 4
Inflammation
Rats
title_short Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
title_full Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
title_fullStr Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
title_full_unstemmed Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
title_sort Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
author Wang,Dong-Xiao
author_facet Wang,Dong-Xiao
Huang,Zheng
Li,Qing-Jie
Zhong,Guo-Qiang
He,Yan
Huang,Wei-Qiang
Cao,Xiao-Li
Tu,Rong-Hui
Meng,Jian-Jun
author_role author
author2 Huang,Zheng
Li,Qing-Jie
Zhong,Guo-Qiang
He,Yan
Huang,Wei-Qiang
Cao,Xiao-Li
Tu,Rong-Hui
Meng,Jian-Jun
author2_role author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Wang,Dong-Xiao
Huang,Zheng
Li,Qing-Jie
Zhong,Guo-Qiang
He,Yan
Huang,Wei-Qiang
Cao,Xiao-Li
Tu,Rong-Hui
Meng,Jian-Jun
dc.subject.por.fl_str_mv HSP90 Heat-Shock Proteins
Ischemic Postconditioning
MAP Kinase Kinase 4
Inflammation
Rats
topic HSP90 Heat-Shock Proteins
Ischemic Postconditioning
MAP Kinase Kinase 4
Inflammation
Rats
description Abstract Purpose To investigate whether heat shock protein 90 (HSP90) is involved in complement regulation in ischemic postconditioning (IPC). Methods The left coronary artery of rats underwent 30 min of occlusion, followed by 120 min of reperfusion and treatment with IPC via 3 cycles of 30s reperfusion and 30s occlusion. The rats were injected intraperitoneally with 1 mg/kg HSP90 inhibitor geldanamycin (GA) after anesthesia. Eighty rats were randomly divided into four groups: sham, ischemia-reperfusion (I/R), IPC and IPC + GA. Myocardial infarct size, apoptosis index and the expression of HSP90, C3, C5a, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1β and c-Jun N-terminal kinase (JNK) were assessed. Results Compared with the I/R injury, the IPC treatment significantly reduced infarct size, release of troponin T, creatine kinase-MB, and lactate dehydrogenase, and cardiomyocyte apoptosis. These beneficial effects were accompanied by a decrease in TNF-α, IL-1β, C3, C5a and JNK expression levels. However, all these effects were abrogated by administration of the HSP90 inhibitor GA. Conclusion HSP90 exerts a profound effect on IPC cardioprotection, and may be linked to the inhibition of the complement system and JNK, ultimately attenuating I/R-induced myocardial injury and apoptosis.
publishDate 2020
dc.date.none.fl_str_mv 2020-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100201
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100201
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/s0102-865020200010000005
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
publisher.none.fl_str_mv Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
dc.source.none.fl_str_mv Acta Cirúrgica Brasileira v.35 n.1 2020
reponame:Acta Cirúrgica Brasileira (Online)
instname:Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)
instacron:SBDPC
instname_str Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)
instacron_str SBDPC
institution SBDPC
reponame_str Acta Cirúrgica Brasileira (Online)
collection Acta Cirúrgica Brasileira (Online)
repository.name.fl_str_mv Acta Cirúrgica Brasileira (Online) - Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (SBDPC)
repository.mail.fl_str_mv ||sgolden@terra.com.br
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