hes1 [Neurosurgery Wiki]

This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong.
In a study, Wu et al. used the transient [[middle cerebral artery occlusion]] (tMCAO) [[mice]] [[model]] to investigate the role of circCCDC9 in [[stroke pathogenesis]]. They found that the expression of [[circCCDC9]] was significantly decreased in the brains of tMCAO mice. The [[Evans blue]] and brain water content were significantly higher in the Pre-IR and Pre-IR+Vector mice, while these patterns were partially reversed by overexpression of circCCDC9. The [[nitrite]] content and eNOS expression were decreased in the Pre-IR and Pre-IR+Vector groups, which was restored by circCCDC9 overexpression. Overexpression of circCCDC9 also inhibited the expression of [[Caspase 3,]] [[Bax]]/[[Bcl-2]] ratio and the expression of [[Notch1]], [[NICD]] and [[Hes1]] in tMCAO mice. [[Knockdown]] of circCCDC9 increased the expression of [[Caspase]]-3, Bax/Bcl-2 ratio, and the expression of Notch1, NICD, and Hes1. In summary, overexpression of circCCDC9 protected the [[blood-brain barrier]] and inhibited [[apoptosis]] by suppressing the Notch1 signaling pathway, while knockdown of circCCDC9 had the opposite effects. The findings showed that circCCDC9 is a potential novel therapeutic target for cerebrovascular protection in [[acute ischemic stroke]]
((Wu L, Xu H, Zhang W, Chen Z, Li W, Ke W. Circular RNA circCCDC9 alleviates ischaemic stroke ischaemia/reperfusion injury via the Notch pathway. J Cell Mol Med. 2020 Oct 29. doi: 10.1111/jcmm.16025. Epub ahead of print. PMID: 33124180.)).