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Effects of miR‐541 on neurite outgrowth during neuronal differentiation
Author(s) -
Zhang Jun,
Zhang Jing,
Liu Lihong,
Zhou Yang,
Li Yiping,
Shao Zhihua,
Wu Youjun,
Li Mengjie,
Fan Yingying,
Shi Hongjun
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1747
Subject(s) - neurite , synapsin i , gene knockdown , downregulation and upregulation , synapsin , microrna , microbiology and biotechnology , biology , gene expression , nerve growth factor , rna interference , neuron , regulation of gene expression , gene , rna , neuroscience , genetics , in vitro , vesicle , receptor , synaptic vesicle , membrane
MicroRNA (miRNAs) are short non‐coding RNA molecules that downregulate gene expression at post‐transcriptional level. miRNAs are post‐transcriptional regulators of gene expression important for neuron development and function. This report demonstrated that a putative and chemically synthesized miRNA rno‐mir‐541 played an important role in the neuron development. Differentiation of PC12 cells with nerve growth factor (NGF) is associated with neurite outgrowth, a process that involves upregulation of Synapsin I. We predicted, detected and assessed the expression levels of a number of possible miRNAs for synapsin I in rats and our outcomes showed that rno‐mir‐541 was associated with rat synapsin I expression. miR‐541, a brain specific miRNA, plays an important role in repressing neurite extension in cultured PC12 neurons. The neurites of PC12 cells was shortened drasticly as a result of the overexpression of rno‐mir‐541. In contrast, the neurites of PC12 cell developed well after the knockdown of rno‐mir‐541 by RNA interference. Our study showed that rno‐mir‐541 played an important role in neuron‐cell proliferation and neurite outgrowth through suppressing the expression of its target gene synapsin I . Furthermore, the introduction of NGF causes downregulation of miR‐541, de‐repression of its target, Synapsin‐I and allows for neuritogenesis. Thus, miR‐541 functions in neuronal precursors as an endogenous conditional component between NGF and Synapsin‐I. Copyright © 2011 John Wiley & Sons, Ltd.