SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway.
SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway.
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DOI:
10.26355/eurrev_201805_14975
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发表时间:
2018-05
影响因子:
3.3
通讯作者:
Yijian Zhang;Zheng Lm;Wang Cx;Gu Jm;S. Xue
中科院分区:
文献类型:
--
作者:
Yijian Zhang;Zheng Lm;Wang Cx;Gu Jm;S. Xue
OBJECTIVE To investigate whether SENP3 protects H9C2 cells from apoptosis triggered by H/R through the signal transducer and activator of transcription 3 (STAT3) pathway. MATERIALS AND METHODS Male C57BL mice were cultured and mouse models of myocardial I/RI were established. At the same time, cardiomyoblast H9C2 cell line of rat embryo was cultured. Reactive oxygen species (ROS) level was detected during H/R using 2',7'-dichlorofluorescein diacetate (DCFH) kit. Apoptotic cells were checked by flow cytometry. The expressions of p-JAK2, JAK2, STAT3, p-STAT3, cleaved-caspase3 (c-caspase3), and Bcl/Bax were detected using Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS We revealed that SENP3 rose in mice of I/R group and in H9C2 cells following H/R with an increase in p-STAT3. Furthermore, increased expression of SENP3 was found to be dependent on the generation of ROS, as the SENP3 accumulation was inhibited by antioxidant (NAC). Inhibition of SENP3 suppressed the p-STAT3 expression, but promoted cell apoptosis, c-caspase3 expression, and Bcl/Bax ratio. Besides, SENP3 overexpression alleviated the cell apoptosis, which was abrogated by AG490. CONCLUSIONS SENP3 could protect H9C2 against H/R through enhancing JAK2/STAT3 pathway.