Interleukin 35 protects cardiomyocytes following ischemia/reperfusion-induced apoptosis via activation of mitochondrial STAT3
| Autor: | Jiancheng Xiu, Xiangqi Lu, Yangping Chen, Ting Feng, Xinlu Zhang, Fengyun Zhou, Huicheng Wang, Qiuxia Zhang |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
STAT3 Transcription Factor
0301 basic medicine Biophysics Apoptosis Myocardial Reperfusion Injury 030204 cardiovascular system & hematology Mitochondrion Biochemistry Mitochondria Heart Mitochondrial Proteins Mice 03 medical and health sciences 0302 clinical medicine medicine Animals Myocytes Cardiac Viability assay chemistry.chemical_classification Reactive oxygen species biology Interleukins Cytochrome c Interleukin General Medicine medicine.disease Cell biology 030104 developmental biology chemistry biology.protein Signal transduction Reperfusion injury |
| Zdroj: | Acta Biochimica et Biophysica Sinica. 53:410-418 |
| ISSN: | 1672-9145 |
| DOI: | 10.1093/abbs/gmab007 |
| Popis: | Mitochondrial reactive oxygen species (mtROS)-induced apoptosis has been suggested to contribute to myocardial ischemia/reperfusion injury. Interleukin 35 (IL-35), a novel anti-inflammatory cytokine, has been shown to protect the myocardium and inhibit mtROS production. However, its effect on cardiomyocytes upon exposure to hypoxia/reoxygenation (H/R) damage has not yet been elucidated. The present study aimed to investigate the potential protective role and underlying mechanisms of IL-35 in H/R-induced mouse neonatal cardiomyocyte injury. Mouse neonatal cardiomyocytes were challenged to H/R in the presence of IL-35, and we found that IL-35 dose dependently promotes cell viability, diminishes mtROS, maintains mitochondrial membrane potential, and decreases the number of apoptotic cardiomyocytes. Meanwhile, IL-35 remarkably activates mitochondrial STAT3 (mitoSTAT3) signaling, inhibits cytochrome c release, and reduces apoptosis signaling. Furthermore, co-treatment of the cardiomyocytes with the STAT3 inhibitor AG490 abrogates the IL-35-induced cardioprotective effects. Our study identified the protective role of IL-35 in cardiomyocytes following H/R damage and revealed that IL-35 protects cardiomyocytes against mtROS-induced apoptosis through the mitoSTAT3 signaling pathway during H/R. |
| Databáze: | OpenAIRE |
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