Abstract:
:The loss of pancreatic islet β-cell function represents the classical feature in the pathogenesis of type 2 diabetes mellitus (T2DM). Previous evidence has highlighted the involvement of the activated JNK pathway in relation to islet β-cell apoptosis. Hence, during the present study a streptozotocin-induced DM mice model was established in a bid to ascertain as to whether microRNA-30d (miR-30d) plays a regulatory role in the JNK pathway in relation to islet β-cell dysfunction. The collection and identification of the islet β cells from streptozotocin-induced mice was performed. Islet β cells with elevated or suppressed levels of miR-30 as well as knocked down SOCS3 were established in order to verify the regulatory mechanisms by which miR-30d governs SOCS3 in vitro. We found miR-30d was overexpressed among tissue samples obtained form streptozotocin-induced mice and their islet β cells, as well as increasing miR-30d expression when the JNK pathway was activated were found to promote islet β cell growth and cell cycle entry, and inhibit apoptosis. SOCS3, confirmed to be a miR-30d target, was decreased in the islet β cells following the promotion of miR-30d, while the JNK pathway was inhibited following SOCS3 knocdown. Furthermore, the effect of miR-30d inhibition was lost in islet β cells when SOCS3 was knocked down. The data of the present study support the notion that miR-30d-mediated direct suppression of SOCS3 acts to protect pancreatic β-cell functions through the JNK signaling pathway, emphasizing the potential of miR-30d as a novel pharmacological target for treatment and intervention of DM.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Wang S,Wen X,Han XR,Wang YJ,Shen M,Fan SH,Zhuang J,Xu W,Zhang ZF,Shan Q,Li MQ,Hu B,Sun CH,Wu DM,Lu J,Zheng YLdoi
10.1002/jcp.26569subject
Has Abstractpub_date
2018-09-01 00:00:00pages
7343-7355issue
9eissn
0021-9541issn
1097-4652journal_volume
233pub_type
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