Abstract：
:Oxidative stress is believed to be a significant cause of Parkinson's disease (PD). DJ-1 is thought to be an oxidative sensor that protects cells from oxidative insult. It was reported that the level of total DJ-1 protein was significantly reduced in the substantia nigra of sporadic PD patients, suggesting that abnormal DJ-1 expression might contribute to PD pathogenesis. However, the molecular mechanisms underlying the regulation of DJ-1 expression are still not fully explored. As a post-transcriptional regulation of target gene expression, the roles of microRNAs in development and disease progression have received widespread concerns. Therefore, we hypothesized that microRNAs might participate in the regulation of the DJ-1 expression. In the present study, we found that miR-494 could bind to the 3'UTR of DJ-1. Overexpression of miR-494 significantly decreased the level of DJ-1 in vitro and rendered cells more susceptible to oxidative stress. In a MPTP mouse model, overexpression of miR-494 negatively regulated DJ-1 levels and exacerbated MPTP-induced neurodegeneration, as illustrated by the loss of dopaminergic neurons. In conclusion, upregulation of miR-494 contributed to oxidative stress induced neuronal death by inhibiting expression of DJ-1.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Xiong R,Wang Z,Zhao Z,Li H,Chen W,Zhang B,Wang L,Wu L,Li W,Ding J,Chen Sdoi
10.1016/j.neurobiolaging.2013.09.027subject
Has Abstractpub_date
2014-03-01 00:00:00pages
705-14issue
3eissn
0197-4580issn
1558-1497pii
S0197-4580(13)00429-6journal_volume
35pub_type
杂志文章abstract：:The aim of this study was to estimate the number of new cells and neurons added to the dentate gyrus across the lifespan, and to compare the rate of age-associated decline in neurogenesis across species. Data from mice (Mus musculus), rats (Rattus norvegicus), lesser hedgehog tenrecs (Echinops telfairi), macaques (Mac...
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