miR-217 Is a Useful Diagnostic Biomarker and Regulates Human Podocyte Cells Apoptosis via Targeting TNFSF11 in Membranous Nephropathy

Li, Jing; Liu, Bin; Xue, Hen; Zhou, Qiao; Peng, Ling

doi:10.1155/2017/2168767

Cited by 28 publications

(40 citation statements)

References 37 publications

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“…By modulating human podocyte apoptosis through targeting TNFSF11, miR‐217 has been reported as a useful diagnostic biomarker in membranous nephropathy (Li et al., ). Besides, miR‐217 is widely implicated in many diseases, functioning as a potential tumour suppressor in osteosarcoma and a diagnostic and prognostic biomarker for chronic pancreatitis and pancreatic ductal adenocarcinoma (Vychytilova‐Faltejskova et al., ; Wei et al., ).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are a class of non‐coding RNAs that negatively regulate gene expression at the post‐transcriptional level, participating in many biological and pathological processes (Bernardo, Ooi, Lin, & McMullen, ). It has been reported that miR‐217 was significantly down‐regulated in the renal tissue and plasma of membranous nephropathy and down‐regulation of miR‐217 induced human podocyte cells apoptosis (Li, Liu, Xue, Zhou, & Peng, ). Through bioinformatics, the complementary base pairs between miR‐217 and TLR4 were found, suggesting potential interaction between them and some influence on podocyte apoptosis and membranous nephropathy progression.…”

Section: Introductionmentioning

confidence: 99%

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Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

Jin

Pan

et al. 2018

Experimental Physiology

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New Findings What is the central question of this study?What is the role of the long non‐coding RNA X‐inactive specific transcript (XIST), which is up‐regulated in injured podocytes and membranous nephropathy, in the pathogenesis of membranous nephropathy? What is the main finding and its importance?XIST was up‐regulated in kidney tissue with membranous nephropathy and in injured podocytes. Down‐regulation of XIST inhibited podocyte apoptosis. XIST negatively regulated miR‐217, and miR‐217 modulated Toll‐like receptor 4. Inhibition of XIST suppressed podocyte apoptosis induced by angiotensin II via miR‐217. Abstract Membranous nephropathy is often characterized by glomerular podocyte injury. Up‐regulation of the long non‐coding RNA (lncRNA) X‐inactive specific transcript (XIST) has been verified in membranous nephropathy and in injured podocytes. Here the role of XIST in podocyte injury and membranous nephropathy was explored. Quantitative real‐time PCR and western blot were performed to detect the expression of XIST and miR‐217, and Toll‐like receptor 4 (TLR4) protein, respectively. Podocyte apoptosis was evaluated with flow cytometry. Interaction between XIST and miR‐217 was analysed by RNA immunoprecipitation and RNA pull‐down assay. A dual luciferase reporter assay was used to examine the interplay between miR‐217 and TLR4. Up‐regulation of the lncRNA XIST and angiotensin II (Ang II) and kidney and podocyte injury were indicated in kidney tissue of patients with membranous nephropathy. Increase of XIST and apoptosis were induced by Ang II in podocytes. Down‐regulation of XIST reversed podocyte apoptosis induced by Ang II. MiR‐217 was negatively regulated by XIST. MiR‐217 controlled TLR4 by targeting its 3′‐untranslated region. XIST modulated TLR4 through miR‐217 and inhibition of XIST reduced podocyte apoptosis induced by Ang II via regulating miR‐217. Down‐regulation of XIST ameliorates podocyte apoptosis via the miR‐217–TLR4 pathway, which may improve membranous nephropathy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

Jin

Pan

et al. 2018

Experimental Physiology

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“…Differentially expressed miRNAs has been found to be commonly presented in human diseases, including MN [28]. The circulating miRNAs associated with a specific pathophysiological state have been demonstrated as the useful diagnostic biomarkers for MN, such as miR-217 [11]. In addition, recent studies reported that miR-186 was significantly down-regulated in renal tissue from MN patients that contributed to podocytes apoptosis [12].…”

Section: Discussionmentioning

confidence: 99%

“…Increasing studies showed a close connection between abnormal miRNAs and MN progression. For example, the relative expression of miR-217 was significantly downregulated in the tissue and plasma of MN patients and the receiver operating characteristic (ROC) curve analysis indicated that miR-217 might serve as a useful diagnostic biomarker for MN [11]. Both miR-217 and miR-186 were reported to be related with podocytes apoptosis in MN [11,12].…”

Section: Introductionmentioning

confidence: 99%

MiR-130a-5p prevents angiotensin II-induced podocyte apoptosis by modulating M-type phospholipase A2 receptor

Liu

Wang

et al. 2018

Cell Cycle

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Podocyte apoptosis is considered as the important element that promotes the development and progress of membranous nephropathy (MN). Unfortunately, the underlying mechanism of podocytes apoptosis in MN remains elusive. We compared the renal expressions of miR-130a-5p and M-type phospholipase A2 receptor (PLA2R) between MN patients (n = 30) and 30 controls by qRT-PCR and western blot, respectively. The podocyte damage model in vitro was established by angiotensin II (Ang II, 100 nmol/L) exposure for 24 h. Interaction between miR-130a-5p and PLA2R was determined using dual-luciferase reporter gene assay. MN mice were induced by intravenous injection of cBSA. In this study, miR-130a-5p expression was significantly decreased both in the renal biopsy specimens from MN patients and podocyte cell line AB8/13 following stimulation of Ang II. Overexpressed miR-130a-5p in AB8/13 cells significantly attenuated the Ang II induced-apoptosis in vitro. In contrast, down-regulated miR-130a-5p induced podocyte apoptosis. PLA2R was identified as the target of miR-130a-5p in AB8/13 cells. And up-regulated or down-regulated PLA2R could obviously attenuate the effect of miR-130a-5p overexpression or knockdown on the apoptosis of AB8/13 cells. Furthermore, it was also observed that overexpressed miR-130a-5p by miR-130a-5p agomir could obviously alleviate renal injury in MN mice. In conclusion, decreased miR-130a-5p was contributed to the pathological mechanism of MN through increasing PLA2R expression, which induced podocyte apoptosis.

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“…Hence, better understanding of the potential mechanisms on PDLSCs differentiation could be helpful for the treatment of periodontitis. diseases, such as chronic heart failure (Nie et al, 2018), membranous nephropathy (Li et al, 2017), neuropathic pain (Jiang et al, 2019) and malignant tumor (Zhu et al, 2016, Nishioka et al, 2014, Zhao et al, 2010. However, the role of miR-217 on the osteogenesis differentiation of PDLSCs is unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR-217 Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells Though EZH2-mediated Epigenetically Regulating Wnt Pathway

Jiang

Jia

2020

Preprint

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Background: This study aimed to investigate the potential roles of miR-217 and EZH2 in the osteogenic differentiation of PDLSCs.Methods: The expression pattern of miR-217 and EZH2 in PDLSCs during osteogenesis was detected by qRT-PCR. Then gain-and loss-of-function was performed to confirm the roles of miR-217 and EZH2 in the osteogenic differentiation of PDLSCs. Alkaline phosphatase and alizarin red S staining were used to detect the activity of osteoblasts and mineral deposition. Western blot and qRT-PCR were performed to detected osteogenic markers to conform osteogenesis phenotype. Furthermore, dual luciferase reporter assay was conducted to analyze the binding of miR-217 to EZH2. Chromatin immunoprecipitation analysis were performed to explore the mechanism of EZH2 and miR-217 on Wnt pathway.Results: miR-217 was significantly upregulated during the osteogenic differentiation, whereas EZH2 was significantly downregulated. Moreover, knockdown of miR-217 and overexpression of EZH2 inhibited the ALP activity, ARS staining, and expression of osteogenic genes. Furthermore, overexpression of EZH2 partially reversed the effects of miR-217 overexpression on osteoblast differentiation. Finally, miR-217 overexpression promoted the expression of Wnt genes, resulting in the activation of the Wnt/β-catenin signaling pathway by targeting EZH2.Conclusion: Our results demonstrated that miR-217 is induced by osteogenic stimuli and promotes osteogenic differentiation partly by targeting the EZH2/Wnt1/β-Catenin signaling pathway. This study provides a novel understanding of the mechanisms of osteogenic differentiation, and suggests a potential method for promoting bone formation.

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miR-217 Is a Useful Diagnostic Biomarker and Regulates Human Podocyte Cells Apoptosis via Targeting TNFSF11 in Membranous Nephropathy

Cited by 28 publications

References 37 publications

Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

Down‐regulation of the long non‐coding RNA XIST ameliorates podocyte apoptosis in membranous nephropathy via the miR‐217–TLR4 pathway

MiR-130a-5p prevents angiotensin II-induced podocyte apoptosis by modulating M-type phospholipase A2 receptor

MiR-217 Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells Though EZH2-mediated Epigenetically Regulating Wnt Pathway

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