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.
Highlights
Type 2 diabetes mellitus (T2DM) is a prevalent chronic disease among the aging population, often accompanied by co-morbidities and geriatric syndromes [1]
Our results revealed that in comparison with the normal group, there was a significant increase in random blood glucose (RBG) and oral glucose tolerance test (OGTT) in the T2DM group (p < 0.05; Figure 1A)
Thereafter, insulin sensitivity in the rat groups was assessed, which revealed that steady-state plasma glucose (SSPG) concentration of rats in the normal group was (10.9 ± 3.5) mmol/L, whereas in the T2DM group, it was (21.4 ± 7.5) mmol/L (Figure 1C)
Summary
Type 2 diabetes mellitus (T2DM) is a prevalent chronic disease among the aging population, often accompanied by co-morbidities and geriatric syndromes [1]. Heart disease, including heart failure, have been shown to be a major cause of death in T2DM patients [3]. Effects of miR-216a-3p on T2DM energy substrate metabolism are potential indicators of heart failure and are associated with heart energy deficiency [4]. T2DM is the most common and complex type of diabetes mellitus and is primarily caused by pancreatic β cell dysfunction [5, 6]. Changes in cardiac metabolism are considered to be an indication of the shift from glucose to fatty acid metabolism in T2DM [8]. Type 2 diabetes mellitus (T2DM) is a chronic, hyperglycemia-associated, metabolic disorder. 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
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