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- Title
LncRNA MEG3 participates in neuronal cell injury induced by subarachnoid hemorrhage via inhibiting the Pi3k/Akt pathway.
- Authors
LIANG, Z.; CHI, Y.-J.; LIN, G.-Q.; XIAO, L.-F.; SU, G.-L.; YANG, L.-M.
- Abstract
OBJECTIVE: To explore the effect of LncRNA MEG3 in the subarachnoid hemorrhage (SAH) and its underlying mechanism. PATIENTS AND METHODS: The expressions of lncRNA MEG3 in SAH patients and animal model were detected by quantitative real-time PCR (qRT-PCR). After LncRNA MEG3 was overexpressed in neurons by lentivirus, viability and apoptosis abilities were detected by cell counting kit-8 (CCK-8) assay, flow cytometry, and TUNEL assay, respectively. The apoptosis-related genes and Pi3k/Akt pathway-related proteins were further detected by a Western blot. RESULTS: The expressions of lncRNA MEG3 in SAH patients were remarkably higher than normal controls, which were positively correlated with SAH severity. After lncRNA MEG3 overexpression, neuronal cell activity was decreased and cell apoptosis was increased. Moreover, the expressions of Bax, p53, and cleaved Caspase-3 were increased, whereas the expression of Bcl2 and Pi3k/Akt pathway-related proteins were decreased after lncRNA MEG3 overexpression. CONCLUSIONS: LncRNA MEG3 is up-regulated in SAH, which may promote SAH-induced neuronal cell injury via inhibition of the Pi3k/Akt pathway.
- Subjects
LINCRNA; NEURONS; SUBARACHNOID hemorrhage; APOPTOSIS; GENETIC overexpression; PROTEIN genetics; WOUNDS &; injuries
- Publication
European Review for Medical & Pharmacological Sciences, 2018, Vol 22, Issue 9, p2824
- ISSN
1128-3602
- Publication type
Article