LAUSR

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.