| Literature DB >> 25665754 |
H Zou1, Y Ding1, K Wang1, E Xiong2, W Peng2, F Du2, Z Zhang2, J Liu3, A Gong4.
Abstract
PTEN serves as an intrinsic brake on neurite outgrowth, but the regulatory mechanism that governs its action is not clear. In the present study, miR-29a was found to increase neurite outgrowth by decreasing PTEN expression. Results showed that miR-92a-1, miR-29a, miR-92b, and miR-29c expression levels increased during nerve growth factor (NGF)-induced differentiation of PC12 cells. Based on in silico analysis of possible miR-29a targets, PTEN mRNA may be a binding site for miR-29a. A protein expression assay and luciferase reporter assay showed that miR-29a could directly target the 3'-UTRs (untranslated regions) of PTEN mRNA and down-regulate the expression of PTEN. PC12 cells infected with lentiviral pLKO-miR-29a showed far higher levels of miR-29a and Akt phosphorylation level than those infected with control. This promoted neurite outgrowth of PC12 cells. Collectively, these results indicate that miR-29a is an important regulator of neurite outgrowth via targeting PTEN and that it may be a promising therapeutic target for neural disease.Entities:
Keywords: Akt; PTEN; miR-29a; miRNA; neurite outgrowth
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Year: 2015 PMID: 25665754 DOI: 10.1016/j.neuroscience.2015.01.055
Source DB: PubMed Journal: Neuroscience ISSN: 0306-4522 Impact factor: 3.590