| First Author | Yang L | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 479 |
| Issue | 2 | Pages | 186-191 |
| PubMed ID | 27613094 | Mgi Jnum | J:239002 |
| Mgi Id | MGI:5824764 | Doi | 10.1016/j.bbrc.2016.09.023 |
| Citation | Yang L, et al. (2016) Long non-coding RNA HOTAIR promotes ischemic infarct induced by hypoxia through up-regulating the expression of NOX2. Biochem Biophys Res Commun 479(2):186-191 |
| abstractText | BACKGROUND: Mounting studies have illustrated an important role of HOTAIR in cancer progress, but few studies have reported its function in brain disease, including nerve cell-associated ischemic infarct. This study aimed to investigate the function of HOTAIR in ischemic infarct, involving its association with the level of NOX2 during hypoxia-induced ischemic infarct. METHODS: Ischemic infarct mice model was established by hypoxia induction, and cerebral dysfunction was evaluated with the surface cerebral blood flow in the ipsilateral hemisphere. HOTAIR expression in isolated infarction lesion and NOX2 protein level in the circulation were detected. HT22 cells were subjected to hypoxia treatment in vitro for functional studies, including TUNEL-positive cells detection for apoptosis analysis. RESULTS: HOTAIR expression was significantly up-regulated in infarction lesion from ischemic infarct mice, in line with increased NOX2 production, while similar results were also observed in hypoxia treated HT22 cells, which was then reversed by HOTAIR interference. Functional studies demonstrated that HOTAIR showed positive regulation on TUNEL-positive cells and apoptosis. Further in vitro study confirmed that HOTAIR silencing could improve cerebral function of ischemic infarct mice, and markedly decreased NOX2 production in the circulation. CONCLUSION: High expression of HOTAIR promoted the onset of ischemic infarct induced by hypoxia. Moreover, the finding showed that HOTAIR promoted ischemic infarct induced by hypoxia through regulating NOX2 expression, which could add our understanding of the molecular mechanisms in ischemic infarct. |
