SIRT3 protects bovine mammary epithelial cells from heat stress damage by activating the AMPK signaling pathway
| Autor: | Yumeng Xi, Hong Lin, Xiao-Chun Sun, Zhaoyu Han, Yue Wang, Kun-Lin Chen, Hanfang Zeng |
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| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
Gene knockdown QH573-671 SIRT3 Chemistry Immunology Neoplasms. Tumors. Oncology. Including cancer and carcinogens AMPK Cell Biology medicine.disease_cause Article Hsp70 Cell biology Cellular and Molecular Neuroscience mitochondrial fusion Cell death and immune response cardiovascular system medicine Phosphorylation Mitochondrial fission Gene expression Cytology RC254-282 Oxidative stress |
| Zdroj: | Cell Death Discovery, Vol 7, Iss 1, Pp 1-11 (2021) Cell Death Discovery |
| ISSN: | 2058-7716 |
| Popis: | With global warming, heat stress has become an important challenge for the global dairy industry. Sirtuin 3 (SIRT3), an important mitochondrial NAD+dependent decarboxylase and a major regulator of cellular energy metabolism and antioxidant defense, is integral to maintaining normal mitochondrial function. The aim of this study was to assess the protective effect of SIRT3 on damage to bovine mammary epithelial cells (BMECs) induced by heat stress and to explore its potential mechanism. Our results indicate that SIRT3 is significantly downregulated in heat-stressed mammary tissue and high-temperature-treated BMECs. SIRT3 knockdown significantly increased the expression of HSP70, Bax, and cleaved-caspase 3 and inhibited the production of antioxidases, thus promoting ROS production and cell apoptosis in BMECs. In addition, SIRT3 knockdown can aggravate mitochondrial damage by mediating the expression of genes related to mitochondrial fission and fusion, including dynamin-related protein 1, mitochondrial fission 1 protein, and mitochondrial fusion proteins 1and 2. In addition, SIRT3 knockdown substantially decreased AMPK phosphorylation in BMECs. In contrast, SIRT3 overexpression in high-temperature treatment had the opposite effect to SIRT3 knockdown in BMECs. SIRT3 overexpression reduced mitochondrial damage and weakened the oxidative stress response of BMECs induced by heat stress and promoted the phosphorylation of AMPK. Taken together, our results indicate that SIRT3 can protect BMECs from heat stress damage through the AMPK signaling pathway. Therefore, the reduction of oxidative stress by SIRT3 may be the primary molecular mechanism underlying resistance to heat stress in summer cows. |
| Databáze: | OpenAIRE |
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