| Autor: |
Li, Hongbin, Niu, Xiaoxuan, Shi, Huijuan, Feng, Min, Du, Yuming, Sun, Rongqing, Ma, Ning, Wang, Haili, Wei, Dan, Gao, Min |
| Zdroj: |
Laboratory Investigation; September 2022, Vol. 102 Issue: 9 p945-956, 12p |
| Abstrakt: |
Circular RNAs (circRNAs) play important roles in many lung diseases. This study aimed to investigate the role of circHECTD1in acute lung injury (ALI). The mouse and cell models of ALI were induced by lipopolysaccharide (LPS). The apoptosis of alveolar epithelial cells (AECs) was detected by flow cytometry. The relationships between circHECTD1, miRNAs, and target genes were assessed by RNA pull-down, luciferase reporter gene, and RNA-FISH assays. circHECTD1was downregulated in LPS-induced human and mouse AECs (HBE and MLE-12). The knockdown of circHECTD1increased the apoptotic rates and the expressions of miR-136and miR-320a, while its overexpression caused opposite effects in LPS-induced HBE and MLE-12 cells. Mechanistically, circHECTD1bound to miR-320aand miR-136. miR-320atargeted PIK3CA and mediated the effect of circHECTD1on PIK3CA expression. miR-136targeted Sirt1 and mediated the effect of circHECTD1on Sirt1 expression. Silencing PIK3CA and/or Sirt1 reversed the effect of circHECTD1overexpression on the apoptosis of LPS-induced HBE and MLE-12 cells. In vivo, overexpression of circHECTD1alleviated the LPS-induced ALI of mice. Our findings suggested that circHECTD1inhibits the apoptosis of AECs through miR-320a/PIK3CA and miR-136/Sirt1 pathways in LPS-induced ALI. |
| Databáze: |
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