RETRACTED: Overexpression of microRNA-216a-3p Accelerates the Inflammatory Response in Cardiomyocytes in Type 2 Diabetes Mellitus by Targeting IFN-α2

Abstract

Background: Type 2 diabetes mellitus (T2DM) is a chronic, hyperglycemia-associated, metabolic disorder. Heart disease is a major complication of T2DM. The present study aimed to explore the effects of miR-216a-3p on cardiomyocyte proliferation, apoptosis, and inflammation in T2DM through the Toll-like receptor (TLR) pathway involving interferon-α2 (IFN-α2) mediation.Methods: T2DM was induced in rats by a high-fat diet, in combination with an intraperitoneal injection of low-dose streptozotocin. ELISAs were conducted to measure inflammatory-related factors in serum. Next, isolated cardiomyocytes were used in loss- and gain-of-function experiments, followed by MTT and flow cytometry assays, conducted to evaluate cell proliferation, cell cycle, and apoptosis.Results: Our results revealed an increase in the inflammatory response in T2DM rat models, accompanied by significantly increased expression of miR-216a-3p and TLR pathway-related genes. However, a decrease in the expression of IFN-α2 was observed. Moreover, the presence of an miR-216a-3p inhibitor and si-IFN-α2 increased the expression of TLR pathway-related genes and cell apoptosis, whereas cell proliferation was significantly decreased in the cardiomyocytes.Conclusion: We found that in T2DM, miR-216a-3p inhibited the proliferation and enhanced the apoptosis of cardiomyocytes and generated an inflammatory response through activation of the TLR pathway and targeting of IFN-α2.

MicroRNA-93-5p participates in type 2 diabetic retinopathy through targeting Sirt1

“…DR, as one of the most severe microvascular complications of T2DM, has been extensively investigated based on the animal models, among which the co-induction of HFD and STZ injection has been the mainstream method to construct the T2DM rat models. [18,19] In this study, miR-93-5p was found to be upregulated in the retina of T2DM models induced by HFD and STZ injection, which was similar in DR patients and high glucose-induced human RPE and ARPE-19 cells in the previous study. [31] The work of Mammadzada P et al indicated that miR-93 was upregulated in proliferative diabetic retinopathy (PDR) vitreous, particularly the vitreous from post-recurrent vitreous hemorrhage (RVH) patients [10].…”

“…Of note, Sirt1 down-regulation has been reported in the retinas of diabetic mice [15][16][17]. In this context, rats were fed with high-fat diet (HFD) and injected with streptozotocin (STZ) to construct the T2DM models [18,19], followed by the intravitreal injection of antagomir NC (negative control), miR-93-5p antagomir, miR-93-5p agomir and/or recombinant Sirt1, and this model could provide the opportunity to investigate the effect of miR-93-5p-targeted Sirt1 on the retinal damage of STZ-induced T2DM rats.…”