MiR‐33‐Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5
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Wiley
2025
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| _version_ | 1867008437348466688 |
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| author | Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu |
| author_facet | Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu |
| collection | Wiley Open Access |
| contents | MiR‐33‐Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5 Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu Journal of Fish Diseases ABSTRACTMicroRNA‐33 (miR‐33) plays a critical role in the regulation of autophagy and inflammatory responses. In this study, C. idella kidney (CIK) cells were transfected with a miR‐33 mimic or inhibitor and Atg5 was overexpressed or silenced to elucidate the regulatory mechanism of miR‐33. Our findings revealed that the miR‐33 mimic significantly decreased the expression of LC3B (a marker of autophagy activation), and the level of autophagy‐related genes (Beclin‐1, Atg5 and LC3‐1) was also significantly downregulated (p < 0.05). Additionally, the miR‐33 mimic promoted the secretion of proinflammatory factors, including TNF‐α, IL‐6, IL‐12 and IL‐1β (p < 0.05). In contrast, the miR‐33 inhibitor significantly enhanced LC3B protein expression and increased the relative expression of Beclin‐1 and Atg5 (p < 0.05). The secretion of proinflammatory factors (TNF‐α, IL‐6 and IL‐12) was significantly reduced (p < 0.05). These results suggested that inhibition of miR‐33 could induce the initiation of autophagy and attenuate the inflammatory response in CIK cells. Furthermore, we identified Atg5 as a direct target gene of miR‐33. Overexpression of Atg5 significantly upregulated the levels of Beclin‐1, Atg5, Atg4C and LC3‐1, along with a reduction in the secretion of proinflammatory factors (TNF‐α, IL‐12 and IL‐1β). Besides, the activities of superoxide dismutase (SOD) and catalase (CAT) were significantly increased (p < 0.05). Conversely, interference with Atg5 expression caused significant downregulation in the expression levels of Beclin‐1, Atg5, Atg12, Atg4C and LC3‐1, resulting in increased secretion of TNF‐α, IL‐12 and IL‐1β and decreased activity of acid phosphatase (ACP) and SOD (p < 0.05). Taken together, these results suggested that inhibition of miR‐33 expression could promote the initiation of autophagy and attenuate the inflammation in CIK cells through targeting Atg5. This study not only enhances the understanding of the mechanism by which miR‐33 regulates autophagy and inflammation in fish but also provides a theoretical foundation and novel insights to improve disease management in the fish aquaculture industry. 10.1111/jfd.14101 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| doi_str_mv | 10.1111/jfd.14101 |
| format | Artículo Open Access |
| id | wiley_oa_10_1111_jfd_14101 |
| institution | Wiley Open Access |
| license_str_mv | http://onlinelibrary.wiley.com/termsAndConditions#vor |
| publishDate | 2025 |
| publisher | Wiley |
| record_format | wiley_oa |
| spellingShingle | MiR‐33‐Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5 Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu Journal of Fish Diseases MiR‐33‐Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5 Lulu Yang Mengjun Lin Weifang Zhao Yuru Zhang Xinxin Xu Xianglin Cao Guoxing Nie Ronghua Lu Journal of Fish Diseases ABSTRACTMicroRNA‐33 (miR‐33) plays a critical role in the regulation of autophagy and inflammatory responses. In this study, C. idella kidney (CIK) cells were transfected with a miR‐33 mimic or inhibitor and Atg5 was overexpressed or silenced to elucidate the regulatory mechanism of miR‐33. Our findings revealed that the miR‐33 mimic significantly decreased the expression of LC3B (a marker of autophagy activation), and the level of autophagy‐related genes (Beclin‐1, Atg5 and LC3‐1) was also significantly downregulated (p < 0.05). Additionally, the miR‐33 mimic promoted the secretion of proinflammatory factors, including TNF‐α, IL‐6, IL‐12 and IL‐1β (p < 0.05). In contrast, the miR‐33 inhibitor significantly enhanced LC3B protein expression and increased the relative expression of Beclin‐1 and Atg5 (p < 0.05). The secretion of proinflammatory factors (TNF‐α, IL‐6 and IL‐12) was significantly reduced (p < 0.05). These results suggested that inhibition of miR‐33 could induce the initiation of autophagy and attenuate the inflammatory response in CIK cells. Furthermore, we identified Atg5 as a direct target gene of miR‐33. Overexpression of Atg5 significantly upregulated the levels of Beclin‐1, Atg5, Atg4C and LC3‐1, along with a reduction in the secretion of proinflammatory factors (TNF‐α, IL‐12 and IL‐1β). Besides, the activities of superoxide dismutase (SOD) and catalase (CAT) were significantly increased (p < 0.05). Conversely, interference with Atg5 expression caused significant downregulation in the expression levels of Beclin‐1, Atg5, Atg12, Atg4C and LC3‐1, resulting in increased secretion of TNF‐α, IL‐12 and IL‐1β and decreased activity of acid phosphatase (ACP) and SOD (p < 0.05). Taken together, these results suggested that inhibition of miR‐33 expression could promote the initiation of autophagy and attenuate the inflammation in CIK cells through targeting Atg5. This study not only enhances the understanding of the mechanism by which miR‐33 regulates autophagy and inflammation in fish but also provides a theoretical foundation and novel insights to improve disease management in the fish aquaculture industry. 10.1111/jfd.14101 http://onlinelibrary.wiley.com/termsAndConditions#vor |
| title | MiR‐33‐Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5 |
| topic | Journal of Fish Diseases |
| url | https://onlinelibrary.wiley.com/doi/10.1111/jfd.14101 |