Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , , , , , , |
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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Acta Cirúrgica Brasileira (Online) |
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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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1752126445484769280 |