Heat shock protein 90/Akt pathway participates in the cardioprotective effect of exogenous hydrogen sulfide against high glucose-induced injury to H9c2 cells
| Autor: | Jianqiang Feng, Longyun Peng, Xin-xue Liao, Xiao Ke, Rui-Xian Guo, Chengheng Hu, Yi-Ying Yang, Wei Zhang, Ruqiong Nie, Jingfu Chen, Liqiu Mo |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cardiotonic Agents Cell Survival Morpholines Cell 030204 cardiovascular system & hematology Cell Line 03 medical and health sciences 0302 clinical medicine Heat shock protein Genetics medicine Animals Myocytes Cardiac HSP90 Heat-Shock Proteins Hydrogen Sulfide PI3K/AKT/mTOR pathway Oncogene Chemistry Cancer General Medicine Cell cycle medicine.disease Molecular medicine Rats Cell biology Glucose 030104 developmental biology medicine.anatomical_structure Chromones Apoptosis Reactive Oxygen Species Corrigendum Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | International Journal of Molecular Medicine |
| ISSN: | 1791-244X 1107-3756 |
| DOI: | 10.3892/ijmm.2017.2891 |
| Popis: | It has been reported that exogenous hydrogen sulfide (H2S) protects against high glucose (HG)-induced cardiac injury and has a modulatory effect on heat shock protein (HSP) and Akt, which play a cardioprotective role. In this study, we examined whether the HSP90/Akt pathway contributes to the protective effects of exogenous H2S against HG-induced injury to H9c2 cardiac cells. Our results revealed that the exposure of H9c2 cardiac cells to 35 mM glucose (HG) for 1 to 24 h decreased the expression of HSP90 and markedly reduced the expression level of phosphorylated (p)-Akt in a time-dependent manner. Co-exposure of the cells to HG and geldanamycin (GA; an inhibitor of HSP90) aggravated the inhibition of the p-Akt expression level by HG. Of note, treatment of the cells with 400 µM NaHS (a donor of H2S) for 30 min prior to exposure to HG significantly attenuated the HG-induced decrease in the expression levels of both HSP90 and p-Akt, along with inhibition of HG-induced cell injury, as indicated by the increase in cell viability and superoxide dismutase (SOD) activity, and by a decrease in the number of apoptotic cells, reactive oxygen species (ROS) generation, as well as by the decreased dissipation of mitochondrial membrance potential (MMP). Importantly, treatment of the cells with GA or LY294002 (an inhibitor of Akt) prior to exposure to NaHS and HG considerably blocked the cardioprotective effects of NaHS against the HG-induced injury mentioned above. On the whole, the findings of this study demonstrate that the inhibition of the HSP90/Akt pathway may be an important mechanism responsible for HG-induced cardiomyocyte injury. We also provide novel evidence that exogenous H2S protects H9c2 cells against HG-induced injury by activating the HSP90/Akt pathway. |
| Databáze: | OpenAIRE |
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