Objective:To study the effect and mechanism of miR-106a on the development of Alzheimer’s disease (AD) induced by amyloid beta protein (Aβ) in primary cultured hippocampus neurons and PC12 cells. Methods:The primary cultured hippocampus neurons and PC12 cells were treated with Aβ. The expression of miR-106a,STAT3 and JAK2 mRNA were detected by RT-PCR,while the expression of STAT3,p-STAT3 and JAK2 protein were evaluated by Western blot. Results:The expression of miR-106a was lower in Aβ-treated primary cultured hippocampus neurons and PC12 cells than that of controls (P < 0.05). In addition,the expression of STAT3 mRNA and protein was higher in Aβ-treated cells than that of controls (P < 0.05),while the expression of JAK2 showed no significant difference whether Aβ-treated was used or not (P > 0.05). Conclusion:This study suggested that miR-106a might contribute to the pathogenesis of AD by negatively regulating the expression of STAT3.
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Cong Jing, Wang Chaojun, Pu Danhua, Zhang Min, Tan Rongrong, Wu Jie. The effect of miR-106a on amyloid beta protein-induced Alzheimer’s disease in primary cultured hippocampus neurons and PC 12 cells[J].,2013,(11):1493-1496, 1507.