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MiR-384-3p aggravates propofol induced apoptosis in developing neurons by targeting Wnt3a
Abstract
Purpose: To evaluate the cytotoxicity of miR-384-3p toward propofol-treated neonatal rat hippocampal neurons and investigate its related molecular mechanism(s).
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine miR-384-3p expression levels in propofol-treated neonatal rat hippocampal neurons. Cell apoptosis and cell viability were evaluated by flow cytometry analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, respectively. Bioinformatics and dual-luciferase reporter
assay were applied together to forecast and verify the interaction between miR-384-3p and Wnt3a. Wnt3a expression in transfected neonatal rat hippocampal neurons was assessed by Western blot assay.
Results: Propofol induced apoptosis in developing neurons by upregulating miR-384-3p expression levels. Knockdown of miR-384-3p reduced propofol-induced apoptosis in developing neurons. Subsequent experiments indicated that miR-384-3p directly regulated Wnt3a expression via coupling with the 3′-untranslated region of Wnt3a. Furthermore, upregulation of Wnt3a expression levels alleviated propofol-induced cytotoxicity promoted by miR-384-3p (p < 0.01).
Conclusion: MiR-384-3p aggravates propofol-induced apoptosis in developing neurons by targeting Wnt3a.
Keywords: MiR-384-3p, Wnt3a, Propofol, Apoptosis, Developing neurons