Long non-coding RNA CHRF modulates the progression of cerebral ischemia/reperfusion injury via miR-126/SOX6 signaling pathway.

In this study, we found that CHRF was significantly correlated with miR-126, and miR-126 expression was decreased in the ischemic core following ischemia, while CHRF expression was increased according to the in vivo and in vitro experiments. Additionally, miR-126 significantly reduced oxygen-glucose deprivation and reoxygenation (OGD/R)-triggered apoptosis using TUNEL and flow cytometry analysis. Moreover, CHRF played as a competing endogenous RNA (ceRNA) and competed with Sex-determining region Y box 6 (SOX6) to direct binding with miR-126, subsequently regulating ischemic neuronal death. CHRF knockdown in vivo markedly prevented ischemic damage and alleviated neurological dysfunctions. Thereby, these results revealed a new molecular mechanism of lncRNA CHRF through targeting miR-126/SOX6 signaling to modulate ischemic neuronal injury, providing solid evidence to develop promising therapeutic strategies against cerebral ischemic stroke. PMID: 31060778 [PubMed - as supplied by publisher]
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Tags: Biochem Biophys Res Commun Source Type: research