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miR-124 Regulates the Expression of BACE1 in the Hippocampus Under Chronic Cerebral Hypoperfusion.

Authors: Zhang, Xiaowen  Huang, Xiongweiye  Fang, Chen  Li, Qian  Cui, Jing  Sun, Jing  Li, Liang 
Citation: Zhang X, etal., Mol Neurobiol. 2017 May;54(4):2498-2506. doi: 10.1007/s12035-016-9845-y. Epub 2016 Mar 16.
Pubmed: (View Article at PubMed) PMID:26984601
DOI: Full-text: DOI:10.1007/s12035-016-9845-y

Chronic cerebral hypoperfusion (CCH) is a high-risk factor of Alzheimer's disease (AD). MicroRNAs (miRNAs) are ideal mediators of hypoxic stress responses to facilitate cellular adaptation to long-term hypoxia. MiR-124 is a kind of nervous system-specific miRNAs, and one of its target genes is ß-site amyloid precursor protein cleaving enzyme 1 (BACE1). In the present study, miR-124 was found to be inhibited all the time from early to late stage of cerebral hypoxia accompanying with the upregulation of BACE1 protein and overproduction of amyloid-ß (Aß) in the hippocampus from cerebral hypoperfusion rat models. Meanwhile, Aß could further enhance the expression of BACE1 protein due to the inhibition of miR-124. Thus, miR-124 was the key factor in this hypoxia/Aß-miR-124-BACE1-Aß cycle. The activation of EPAC-Rap1 pathway was involved in the inhibition of miR-124 in hippocampus under hypoxia or Aß insult. Our data suggest that, as an endogenous regulator of BACE1 protein, miR-124 may play a role in AD onset induced by CCH.


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CRRD Object Information
CRRD ID: 13782151
Created: 2018-08-23
Species: All species
Last Modified: 2018-08-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.