期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 376, 期 1-2, 页码 189-195出版社
SPRINGER
DOI: 10.1007/s11010-013-1567-0
关键词
NPY; miR-30a-5p; BDNF; Primary cortical neurons; Alzheimer disease
类别
资金
- nEUROsyn Italian Ministry of Health in the frame of ERA-Net Neuron [RC2008]
Using in vitro models of Alzheimer's disease (AD), we found that the toxic effects of amyloid beta 25-35 (A beta(25-35)) on the neurotrophin brain-derived neurotrophic factor (BDNF) were counteracted by pre-incubation with neuropeptide Y (NPY), a neuropeptide expressed within the central nervous system. Nonetheless, the mechanism of action of NPY on BDNF neuronal production in the presence of A beta is not known. BDNF expression might be directly regulated by microRNA (miRs), small non-coding DNA fragments that regulate the expression of target genes. Thus, there is the possibility that miRs alterations are present in AD-affected neurons and that NPY influences miR expression. To test this hypothesis, we exposed NPY-pretreated primary rat cortical neurons to A beta(25-35) and measured miR-30a-5p (a member of the miR-30a family involved in BDNF tuning expression) and BDNF mRNA and protein expression after 24 and 48 h. Our results demonstrated that pre-treatment with NPY decreased miR-30a-5p expression and increased BDNF mRNA and protein expression at 24 and 48 h of incubation with A beta. Therefore, this study demonstrates that NPY modulates BDNF and its regulating microRNA miR-30a-5p in opposite direction with a mechanism that possibly contributes to the neuroprotective effect of NPY in rat cortical neurons exposed to A beta.
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