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MicroRNA‐124 and its target gene are altered in the substantia nigra (SNc) of the brain of MPTP‐mouse model of Parkinson's disease
Author(s) -
Kanagaraj Nandhini,
Dheen S Thameem,
Peng Zhao Feng,
Srinivasan Dinesh Kumar,
Tay Samuel S W
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.83.6
Subject(s) - substantia nigra , mptp , dopaminergic , microrna , parkinson's disease , neuroscience , pathogenesis , biology , pars compacta , dopamine , disease , medicine , gene , pathology , genetics , immunology
MicroRNAs (miRNAs) are small, non‐protein coding RNAs involved in post‐transcriptional gene expression regulation. Several recent studies have demonstrated the importance of miRNAs in diseases of the nervous system. Parkinson's disease (PD) is the second most common neurodegenerative disease characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SNc) of the brain. The involvement of a few miRNAs in PD has been proven to be a promising potential for therapeutic targeting. The brain‐enriched miR‐124 has been shown to play a role in plasticity, inflammation and stress response in the brain. We used the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridinium (MPTP)‐ induced mouse model to study if miR‐124 has any important role in PD pathogenesis and whether it can offer a new therapeutic target. We evaluated the expression of miR‐124 in the SNc of the PD model at different time points by Real‐time PCR. A significant decrease in expression of miR‐124 over time was observed. We also found an increase in the levels of NeuroD1 which has been shown to be a target of miR‐124. Preliminary data from the dopaminergic neuronal (MN9D) cell line treated with MPP iodide also showed a similar pattern. In summary, miR‐124 depletion plays an important role in the pathogenesis of PD. The exact mechanism involved remains to be elucidated. Supported by Grant MOE 2009‐T2‐1‐061 from the Ministry of Education.