Abstract
Diabetic cardiomyopathy (DCM) is one of the most serious complications of diabetes, but its pathogenesis remains largely unclear. In the present study, we aimed to explore the potential role of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and to investigate the underlying mechanisms in human AC16 cardiomyocytes under high glucose (HG) condition. The results demonstrated that MEG3 was overexpressed in HG-treated AC16 cells, and MEG3 knockdown suppressed the HG-induced apoptosis in AC16 cells. Mechanistically, MEG3 directly binds to miR-145 in AC16 cells, thereby up-regulating the expression of PDCD4. Rescue experiments showed that the role of MEG3 in HG-treated AC16 cells was partly dependent on its suppression on miR-145. In summary, our findings suggested that the role of MEG3 in HG-treated human cardiomyocytes is to serve as a competing endogenous RNA (ceRNA), which negatively regulates miR-145. These findings may provide a valuable and promising therapeutic target for the treatment of DCM in the future.
Highlights
Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is an emerging global health problem
Western blot analysis pointed out that the Bcl-2/Bax expression ratio was decreased, whereas the cleaved caspase-3 expression was increased in AC16 cells following 48 h of high glucose (HG) treatment, but these effects were obviously restored by Maternally expressed gene 3 (MEG3) knockdown (Figure 2D)
Some literatures have focused on the regulatory role of long non-coding RNA (lncRNA) in Diabetic cardiomyopathy (DCM)
Summary
Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is an emerging global health problem. Diabetic cardiomyopathy (DCM), a common cardiovascular complication occurring in patients with DM, is featured by early impairments in diastolic function, accompanied by the development of cardiac hypertrophy, myocardial fibrosis, and cardiomyocyte apoptosis [1]. LncRNAs have attracted widespread attention for their regulatory role in a wide range of biological processes and human diseases [3]. Wu et al [5] found a remarkable up-regulation of MEG3 in mouse injured heart after myocardial infarction, and Gong et al [6] reported that knockdown of MEG3 decreased hypoxia-induced injury in rat cardiomyocyte-derived H9c2 cells. Through a series of in vitro experiments, we aimed to investigate the potential regulatory role of MEG3 in human AC16 cardiomyocytes under high glucose (HG) condition
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