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© 2016. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Heat shock protein 70 (HSP70) maintains Ca2+ homeostasis in PC12 cells, which may protect against apoptosis; however, the mechanisms of neuroprotection are unclear. Therefore, in this study, we examined Ca2+ levels in PC12 cells transfected with an exogenous lentiviral HSP70 gene expression construct, and we subsequently subjected the cells to ischemia-hypoxia/reoxygenation injury. HSP70 overexpression increased neuronal viability and ATPase activity, and it decreased cellular reactive oxygen species levels and intracellular Ca2+ concentration after hypoxia/reoxygenation. HSP70 overexpression enhanced the protein and mRNA expression levels of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), but it decreased the protein and mRNA levels of inositol 1,4,5-trisphosphate receptor (IP3R), thereby leading to decreased intracellular Ca2+ concentration after ischemia-hypoxia/reoxygenation. These results suggest that exogenous HSP70 protects against ischemia-hypoxia/reoxygenation injury, at least in part, by maintaining cellular Ca2+ homeostasis, by upregulating SERCA expression and by downregulating IP3R expression.

Details

Title
Heat shock protein 70 protects PC12 cells against ischemia-hypoxia/reoxygenation by maintaining intracellular Ca2+ homeostasis
Author
Liu, Yuan 1 ; Xue-chun, Wang 1 ; Hu, Dan 1 ; Shu-ran Huang 2 ; Qing-shu, Li 1 ; Li, Zhi 1 ; Qu, Yan 1 

 Department of Intensive Care Unit, Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, Shandong Province 
 Department of Intensive Care Unit, Affiliated Hospital of Jining Medical University, Jining, Shandong Province 
Pages
1134-1140
Publication year
2016
Publication date
Jul 2016
Publisher
Medknow Publications & Media Pvt. Ltd.
ISSN
16735374
e-ISSN
18767958
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2382717909
Copyright
© 2016. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.