Journal
FRONTIERS IN MOLECULAR NEUROSCIENCE
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2016.00140
Keywords
Alzheimer's disease (AD); beta amyloid peptide (A beta); microRNA; miR-200c; PTEN; endoplasmic reticulum stress (ER stress)
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Funding
- National Basic Research Program of China (973 Program) [2014CB910204]
- National Key Research and Development Program [2016YFA0501900]
- National Natural Scientific Foundation of China [81300922, 81371737, 81571043]
- Natural Science Foundation of Guangdong Province [2016A030312016]
- Shenzhen Basic Research Grants [JCYJ20140416144209745, JCYJ20160229153100269]
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MicroRNAs are small non-coding RNAs that repress the expression of their target proteins. The roles of microRNAs in the development of Alzheimer's disease (AD) are not clear. In this study we show that miR-200c represses the expression of PTEN protein. PTEN downregulation by miR-200c supports the survival and differentiation of cultured neurons. AD is a progressive neurodegenerative disease signified by beta amyloid (4) peptide aggregation and deposition. In a mouse model of AD that is induced by APPswe and PS1 Delta E9 double transgenes, we found 4 deposition results in neuronal ER stress that induces miR200c. Pharmacological blockade of ER stress inhibited A beta-induced miR-200c overexpression in AD brains. MiR-200c was detected in the serum of both AD mice and human AD patients. These findings suggest that miR-200c functions as part of the neuronal cell-intrinsic adaptive machinery, and supports neuronal survival and differentiation in response to 4 induced ER-stress by downregulating PTEN.
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