Publication:
Downregulation of miR-527 alleviates sepsisinduced acute kidney injury via targeting Beclin1

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Xu-38-443-452-2023.pdf(5.63 MB)
Date
2023
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Authors
Xu, Ke ; Mo, Xiaojun ; Wang, Yijun ; Zeng, Zhenhua ; Xu, Ziqiang ; Yue, Dongyou ; Li, Guicheng ; Li, Tao ; Liu, Junhong ; Yuan, Jiemin
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-531
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info:eu-repo/semantics/article
Description
Abstract
Background. Sepsis-induced acute kidney injury (AKI) is known to result from the inflammatory responses. MiRNAs participate in the development of sepsis-induced AKI. Nevertheless, the function of miR527 in sepsis-induced AKI remains unclear. Methods. Cell viability was evaluated by CCK8 assay, and TUNEL staining was applied to assess cell apoptosis. Pro-inflammatory cytokine (TNF-α, IL-6 and IL-1β) levels were evaluated by ELISA. Meanwhile, the relation among miR-527 and Beclin1 was detected by dual luciferase report assay. Western blot and RT-qPCR were used to examine the protein and mRNA levels, respectively. Furthermore, an in vivo model was constructed to assess the function of miR-527 in sepsisinduced AKI. Results. MiR-527 downregulation significantly alleviated the symptoms of sepsis-induced AKI in mice. MiR-527 level in HK-2 cells was significantly upregulated by LPS, and downregulation of miR-527 notably reversed LPS-induced inhibition of HK-2 cell viability by inhibiting apoptosis. In addition, LPS greatly increased TNF-α, IL-6 and IL-1β levels in supernatant of HK-2 cells, while miR-527 inhibitor partially restored this phenomenon. Meanwhile, Beclin1 was found to be the downstream mRNA of miR-527, and miR-527 inhibitor notably upregulated the level of LC3. MiR-527 downregulation reversed LPS-induced HK-2 cell injury through suppression of TGF-β pathway. Conclusion. Downregulation of miR-527 alleviated sepsis-induced AKI via targeting Beclin1. Thus, miR527 might act as a vital mediator in sepsis-induced AK
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Sepsis , AKI , miR-527 , Beclin1
Citation
Histology and Histopathology Vol. 38, nº4 (2023)
URI
http://hdl.handle.net/10201/129752
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Histology and histopathology Vol.38, nº4 (2023)
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