microRNAs in Diabetic Kidney Disease

Chung, Arthur C.K.

doi:10.1007/978-3-319-22671-2_13

Cited by 22 publications

(16 citation statements)

References 110 publications

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“…Studies have highlighted the critical role of miRs in the progression of renal disease through regulation of target gene expression [44, 45], and SIRT1 was shown to be regulated by miRs [32, 33, 46, 47]. It has been revealed that miR-21 can protect the kidney against ischaemia-reperfusion injury by inhibiting the inflammatory response and apoptosis, which is one of the mechanisms involved in the protective effect of renal ischaemic preconditioning in vivo and in vitro [48, 49].…”

Section: Discussionmentioning

confidence: 99%

MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells

Lin

Geng

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Recent studies have indicated that microRNA-21 (miR-21) is involved in the inflammatory response in relation to renal disease. Sirtuin1 (SIRT1) exerts renoprotective properties by counteracting inflammation. The activation of CD40 triggers inflammation that participates in renal inflammation and injury. The relationship between miR-21, SIRT1 and CD40, however, remains elusive. Methods: Immunohistochemistry, small-interfering RNA (siRNA) transfection, quantitative real-time PCR and western blotting were applied to assess the morphological, functional and molecular mechanisms in primary cultured renal inner medullary collecting duct (IMCD) cells. Results: TNF-α induced miR-21, CD40 and acetylated-NF-κBp65 (Ac-p65) expressions and reduced SIRT1 expression in IMCD cells. miR-21 mimics increased SIRT1 expression and attenuated Ac-p65 and CD40 expressions in TNF-α-induced IMCD cells, and the corresponding changes were observed with a miR-21 inhibitor. SIRT1 overexpression or activation by SRT1720 diminished TNF-α-induced CD40 and Ac-p65 expressions, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol and augmented by pretreatment with NF-κB siRNA. Further study found that the inhibitory effect of miR-21 on Ac-p65 and CD40 expressions was impeded by pretreatment with SIRT1 siRNA. Conclusion: The present study indicates that miR-21 inhibits TNF-α-induced CD40 expression in IMCD cells via the SIRT1-NF-κB signalling pathway, which provides new insight in understanding the anti-inflammatory effect of miR-21.

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Section: Discussionmentioning

confidence: 99%

MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells

Lin

Geng

Zhao

et al. 2017

Cell Physiol Biochem

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“…miRNAs as potential biomarkers. Being key regulators of cellular survival, proliferation, and SM differentiation (21) and of gain or loss of function under physiological and pathophysiological conditions, miRNAs not surprisingly may also serve as novel biomarkers for a number of diseases involving heart, cancer, kidney, autism, Parkinson's disease, depression, peritoneal fibrosis, autoimmunity, and arthritis (3,25,32,35,50,54,96,116,140). Recently, this list has grown to include the role of miRNAs as potential biomarkers in the pathophysiology of different SMs.…”

Section: Role Of Mirnas In Fibrosis Of Gastrointestinal Tract Micrornmentioning

confidence: 99%

Role of microRNAs in gastrointestinal smooth muscle fibrosis and dysfunction: novel molecular perspectives on the pathophysiology and therapeutic targeting

Krishna

Singh

Thangavel

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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MicroRNAs (miRNAs) belong to a group of short noncoding RNA molecules with important roles in cellular biology. miRNAs regulate gene expression by repressing translation or degrading the target mRNA. Recently, a growing body of evidence suggests that miRNAs are implicated in many diseases and could be potential biomarkers. Fibrosis and/smooth muscle (SM) dysfunction contributes to the morbidity and mortality associated with several diseases of the gastrointestinal tract (GIT). Currently available therapeutic modalities are unsuccessful in efficiently blocking or reversing fibrosis and/or SM dysfunction. Recent understanding of the role of miRNAs in signaling pathway of fibrogenesis and SM phenotype switch has provided a new insight into translational research. However, much is still unknown about the molecular targets and therapeutic potential of miRNAs in the GIT. This review discusses miRNA biology, pathophysiology of fibrosis, and aging- associated SM dysfunction in relation to the deregulation of miRNAs in the GIT. We also highlight the role of selected miRNAs associated with fibrosis and SM dysfunction-related diseases of the GIT.

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“…A previous study determined that miR-192 was elevated in DKD via the mediation of renal fibrosis ( 14 ). Additional important miRNAs for DKD progression have also been previously identified, including miR-21, miR-29c, miR-200b, miR-216a and miR-377 ( 15 ).…”

Section: Introductionmentioning

confidence: 98%

Microarray analysis reveals gene and microRNA signatures in diabetic kidney disease

Cui

et al. 2017

Mol Med Report

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The current study aimed to identify therapeutic gene and microRNA (miRNA) biomarkers for diabetic kidney disease (DKD). The public expression profile GSE30122 was used. Following data preprocessing, the limma package was used to select differentially-expressed genes (DEGs) in DKD glomeruli samples and tubuli samples and they were compared with corresponding controls. Then overlapping DEGs in glomeruli and tubuli were identified and enriched analysis was performed. In addition, protein-protein interaction (PPI) network analysis as well as sub-network analysis was conducted. miRNAs of the overlapping DEGs were investigated using WebGestal. A total of 139 upregulated and 28 downregulated overlapping DEGs were selected, which were primarily associated with pathways involved in extracellular matrix (ECM)-receptor interactions and cytokine-cytokine receptor interactions. CD44, fibronectin 1, C-C motif chemokine ligand 5 and C-X-C motif chemokine receptor 4 were four primary nodes in the PPI network. miRNA (miR)-17-5p, miR-20a and miR-106a were important and nuclear receptor subfamily 4 group A member 3 (NR4A3), protein tyrosine phosphatase, receptor type O (PTPRO) and Kruppel like factor 9 (KLF9) were all predicted as target genes of the three miRNAs in the integrated miRNA-target network. Several genes were identified in DKD, which may be involved in pathways such as ECM-receptor interaction and cytokine-cytokine receptor interaction. Three miRNAs may also be used as biomarkers for therapy of DKD, including miR-17-5p, miR-20a and miR-106a, with the predicted targets of NR4A3, PTPRO and KLF9.

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microRNAs in Diabetic Kidney Disease

Cited by 22 publications

References 110 publications

MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells

MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells

Role of microRNAs in gastrointestinal smooth muscle fibrosis and dysfunction: novel molecular perspectives on the pathophysiology and therapeutic targeting

Microarray analysis reveals gene and microRNA signatures in diabetic kidney disease

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