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https://doi.org/10.14670/HH-18-531
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Título: | Downregulation of miR-527 alleviates sepsisinduced acute kidney injury via targeting Beclin1 |
Fecha de publicación: | 2023 |
Editorial: | Universidad de Murcia, Departamento de Biologia Celular e Histiologia |
Cita bibliográfica: | Histology and Histopathology Vol. 38, nº4 (2023) |
ISSN: | 0213-3911 1699-5848 |
Materias relacionadas: | 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 |
Palabras clave: | Sepsis AKI miR-527 Beclin1 |
Resumen: | 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 |
Autor/es principal/es: | Xu, Ke Mo, Xiaojun Wang, Yijun Zeng, Zhenhua Xu, Ziqiang Yue, Dongyou Li, Guicheng Li, Tao Liu, Junhong Yuan, Jiemin |
URI: | http://hdl.handle.net/10201/129752 |
DOI: | https://doi.org/10.14670/HH-18-531 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 10 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.38, nº4 (2023) |
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