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SP1-stimulated miR-208a-5p aggravates sepsis-induced myocardial injury via targeting XIAP.
Xu, Ling-Jun; Yang, Yixian; Yuan, Ling-Feng; Liu, Hong; Xu, Nan-Ping; Yang, Yu; Huang, Liang.
Afiliación
  • Xu LJ; Department of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi Province, PR China; Department of Emergency, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China.
  • Yang Y; Department of Emergency, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China.
  • Yuan LF; Department of Function, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China.
  • Liu H; Department of Emergency, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China.
  • Xu NP; Department of Emergency, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China.
  • Yang Y; Department of Endocrinology, Metabolism and Genetics, Jiangxi Provincial Children's Hospital, Nanchang 330038, Jiangxi Province, PR China. Electronic address: yangyu5168@126.com.
  • Huang L; Department of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi Province, PR China. Electronic address: huangliang6312@sina.com.
Exp Cell Res ; 435(1): 113905, 2024 Feb 01.
Article en En | MEDLINE | ID: mdl-38163563
ABSTRACT
The development of sepsis can lead to many organ dysfunction and even death. Myocardial injury is one of the serious complications of sepsis leading to death. New evidence suggests that microRNAs (miRNAs) play a critical role in infection myocardial injury. However, the mechanism which miR-208a-5p regulates sepsis-induced myocardial injury remains unclear. To mimic sepsis-induced myocardial injury in vitro, rat primary cardiomyocytes were treated with LPS. Cell viability and apoptosis were tested by CCK-8 and flow cytometry, respectively. The secretion of inflammatory factors was analyzed by ELISA. mRNA and protein levels were detected by RT-qPCR and Western blotting. The interaction among SP1, XIAP and miR-208a-5p was detected using dual luciferase report assay. Ultrasonic analysis and HE staining was performed to observe the effect of miR-208a-5p in sepsis-induced rats. Our findings indicated that miR-208a-5p expression in primary rat cardiomyocytes was increased by LPS. MiR-208a-5p inhibitor reversed LPS-induced cardiomyocytes injury through inhibiting the apoptosis. Furthermore, the inflammatory injury in cardiomyocytes was induced by LPS, which was rescued by miR-208a-5p inhibitor. In addition, downregulation of miR-208a-5p improved LPS-induced sepsis myocardial injury in vivo. Mechanistically, XIAP might be a target gene of miR-208a-5p. SP1 promoted transcription of miR-208a by binding to the miR-208a promoter region. Moreover, silencing of XIAP reversed the regulatory of miR-208a-5p inhibitor on cardiomyocytes injury. To sum up, those findings revealed silencing of miR-208a-5p could alleviate sepsis-induced myocardial injury, which would grant a new process for the treatment of sepsis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sepsis / MicroARNs Límite: Animals Idioma: En Revista: Exp Cell Res Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sepsis / MicroARNs Límite: Animals Idioma: En Revista: Exp Cell Res Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos