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MicroRNA-153 negatively regulates the expression of amyloid precursor protein and amyloid precursor-like protein 2.
MedLine Citation:
PMID:  22510281     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Increased expression of the amyloid precursor protein (APP) is a crucial risk factor of Alzheimer's disease (AD). Amyloid precursor-like protein 2 (APLP2), a homologue of APP, is also suggested to participate in AD pathogenesis. Accumulating evidence suggest the regulatory role of microRNA on AD-related genes. Here we showed that the levels of miR-153 were significantly decreased at early- and late-stage of AD in APPswe/PSΔE9 murine model. Moreover, a binding site of miR-153 on APP and APLP2-3'UTR was identified, respectively, by luciferase assay. Gain and loss of function experiments demonstrated that miR-153 suppressed the expression of APP and APLP2. Using miR-153 transgenic mouse model, we testified that miR-153 downregulated the expression of APP and APLP2 protein in vivo. Furthermore, closely related expression patterns of miR-153 and APP/APLP2 during brain development indicated a physiological regulation role of miR-153 on the two genes. In a neuronal cell line treated with Aβ(42) peptides and H(2)O(2,) the levels of miR-153 varied during time-course leading to corresponding changes of APLP2 protein, indicating Aβ peptides and oxidative stress influence the expression of miR-153. Thus, miR-153 contributes to post-transcriptional regulation of APP/APLP2, suggesting a possible role for miR-153 in neuro-pathological conditions.
Authors:
Chunlian Liang; Hua Zhu; Yanfeng Xu; Lan Huang; Chunmei Ma; Wei Deng; Ying Liu; Chuan Qin
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-11-4
Journal Detail:
Title:  Brain research     Volume:  -     ISSN:  1872-6240     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2012-4-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier B.V.
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