MiR-33-Mediated Regulation of Autophagy and Inflammation in CIK Cells Through Atg5.

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Tác giả: Xianglin Cao, Mengjun Lin, Ronghua Lu, Guoxing Nie, Xinxin Xu, Lulu Yang, Yuru Zhang, Weifang Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 579.373 *Irregular, nonsporing, gram-positive rods

Thông tin xuất bản: England : Journal of fish diseases , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 239436

 MicroRNA-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.
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