Abstract:
BACKGROUND:The activation of the Notch signaling pathway has been shown to play an important role in diabetic nephropathy (DN) development. Besides, Notch-1 is a target gene in miR-34a. However, the regulation of the podocyte lesions involved in DN by miR-34a has not been identified. METHODS:This study utilized miR-34a mimics and small interfering RNA transfection to construct miR-34a overexpression and lower-expression model to investigate the effect of miR-34a on the regulation of the Notch signaling pathway and podocyte lesions in DN. Western blotting and real-time quantitative polymerase chain reaction were applied for the quantitative testing of mRNA and protein expression. Apoptosis of podocyte was detected by TUNEL staining. RESULTS:In high-glucose (HG) conditions, miR-34a overexpression inhibited the expression of Notch 1, Jagged 1, NICD, Hes 1, and Hey 1 proteins. Further, cleaved caspase-3, Bax, and phosphorylation of p53 (p-p53) were reduced significantly. Therefore, miR-34a overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG. β-arrestin was slightly reduced in HG conditions. Meanwhile, miR-34a overexpression could remit the inhibition. CONCLUSION:Results from this study provide evidence that miR-34a may offer a new approach for the treatment of diabetes.
journal_name
Medicine (Baltimore)journal_title
Medicineauthors
Zhang X,Song S,Luo Hdoi
10.1097/MD.0000000000005050subject
Has Abstractpub_date
2016-11-01 00:00:00pages
e5050issue
44eissn
0025-7974issn
1536-5964pii
00005792-201611010-00005journal_volume
95pub_type
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