Background: Diabetic nephropathy (DN) is a leading cause of chronic kidney disease and end-stage renal disease worldwide. The maternally expressed gene-3 (Meg3), a lncRNA, is implicated in the development of diabetic microvascular complications like retinopathy and nephropathy. and Transforming Growth Factor-Beta (TGF-β) are established playmakers in fibrogenesis in DN. Research stated that MEG3 can sponge miRNA-21 inhibiting it. Additionally, MEG3 modulates the activity of TGF-β genes by binding to promotor-distal regulatory elements. Aim: Investigate MEG3 regulatory role in DN pathogenesis, and its possible inhibitory effect on miRNA-21 and TGF-β signaling pathways. Methods:The study was performed on 75 subjects divided into 3 groups: 25 controls, 25 diabetics, and 25 DN patients. Participants were subjected to routine laboratory investigations, estimation of gene expression of MEG3 and miRNA-21 by RT-qPCR and measurement of serum TGF-β levels by ELISA. Results: DN group shows a highly significant decrease in MEG-3 relative gene expression, and a significant increase in both miRNA-21 relative gene expression and TGF-β sera levels, when compared to diabetic and control groups. In addition, MEG3 is significantly negatively correlated to miRNA-21, TGF-β1, and HbA1c confirming the sponging effect of MEG3 on miRNA-21 and predicting its potential protective role in DN. On the other hand, there is a statistically significant positive correlation between miRNA-21 gene expression and TGF-β1 levels indicating the up-regulatory role of miRNA-21 on TGF-β1 protein expression levels. Conclusion: Our data suggest that MEG3 is implicated in DN pathogenesis through a possible loop encompassing miRNA-21 and TGF-β1.
Introduction: Diabetic nephropathy (DN) is a leading cause of chronic kidney disease and end-stage renal disease worldwide. The maternally expressed gene-3 (MEG3), a lncRNA, is implicated in the development of diabetic microvascular complications like retinopathy and nephropathy. MicroRNA-21 (miRNA-21) and Transforming Growth Factor-Beta (TGF-β) are established playmakers in fibrogenesis in DN. Research stated that MEG3 can sponge miRNA-21 inhibiting it. Additionally, MEG3 modulates the activity of TGF-β genes by binding to promotor-distal regulatory elements. Aim: Investigate MEG3 regulatory role in DN pathogenesis, and its possible inhibitory effect on miRNA-21 and TGF-β signaling pathway. Methods: The study was performed on 75 subjects divided into 3 groups: 25 controls, 25 diabetics, and 25 DN patients. Participants were subjected to routine laboratory investigations, estimation of gene expression of MEG3 and miRNA-21 by RT-qPCR and measurement of serum TGF-β levels by ELISA. Results: DN group shows a highly significant decrease in MEG-3 relative gene expression, and a significant increase in both miRNA-21 relative gene expression and TGF-β sera levels, when compared to diabetic and control groups. In addition, MEG3 is significantly negatively correlated to miRNA-21, TGF-β1, and HbA1c confirming the sponging effect of MEG3 on miRNA-21 and predicting its potential protective role in DN. On the other hand, there is a statistically significant positive correlation between miRNA-21 gene expression and TGF-β1 levels indicating the up-regulatory role of miRNA-21 on TGF-β1 protein expression levels. Conclusion: Our data suggests that MEG3 is implicated in DN pathogenesis through a possible loop encompassing miRNA-21 and TGF- β1.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.