Genetic susceptibility to idiopathic membranous nephropathy in high-prevalence Area, Taiwan

Chen, Shih Yin; Chen, Cheng Hsu; Huang, Yu Chuen; Chan, Chia Jung; Chen, Da Chung; Tsai, Fuu Jen

doi:10.7603/s40681-014-0009-y

Cited by 14 publications

(8 citation statements)

References 56 publications

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“…The expression of mRNAs encoding TLR4 was increased in IgA nephropathy, which presented with immune deposits of IgA within glomeruli (Donadio et al., ). Subsequently, TLR4 was claimed to be associated with membranous nephropathy, which is considered a non‐inflammatory organ‐specific autoimmune disease (Chen et al., ). The current study emphasized the effect of TLR4 on membranous nephropathy progression by affecting podocyte apoptosis.…”

Section: Discussionmentioning

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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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%

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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“…However, there are reports of a genetic susceptibility to idiopathic membranous nephropathy. This type of study was conducted in a high-prevalence area in Taiwan [97]. In these studies, the association of the IL-6, NPHS1 (nephrin), TLR-4, TLR-9, STAT4 (signal transducer and activator of transcription) and MYH (mutY DNA glycosylase), genes with susceptibility to primary membranous nephropathy in Taiwan was established.…”

Section: Membranous Nephropathy (Mn)mentioning

confidence: 99%

Toll-Like Receptor as a Potential Biomarker in Renal Diseases

Mertowski

Lipa

Morawska

et al. 2020

IJMS

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One of the major challenges faced by modern nephrology is the identification of biomarkers associated with histopathological patterns or defined pathogenic mechanisms that may assist in the non-invasive diagnosis of kidney disease, particularly glomerulopathy. The identification of such molecules may allow prognostic subgroups to be established based on the type of disease, thereby predicting response to treatment or disease relapse. Advances in understanding the pathogenesis of diseases, such as membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis, IgA (immunoglobulin A) nephropathy, and diabetic nephropathy, along with the progressive development and standardization of plasma and urine proteomics techniques, have facilitated the identification of an increasing number of molecules that may be useful for these purposes. The growing number of studies on the role of TLR (toll-like receptor) receptors in the pathogenesis of kidney disease forces contemporary researchers to reflect on these molecules, which may soon join the group of renal biomarkers and become a helpful tool in the diagnosis of glomerulopathy. In this article, we conducted a thorough review of the literature on the role of TLRs in the pathogenesis of glomerulopathy. The role of TLR receptors as potential marker molecules for the development of neoplastic diseases is emphasized more and more often, as prognostic factors in diseases on several epidemiological backgrounds.

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“…In recent years, numerous studies have indicated that certain genetic polymorphisms associated with susceptibility to this disease. [ 5 , 6 ] And this discovery has opened a new horizon in the therapy of iMN.…”

Section: Introductionmentioning

confidence: 99%

Association between the HLA-DQA1 rs2187668 polymorphism and risk of idiopathic membranous nephropathy

Bao

et al. 2018

Medicine

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Objective:Numerous studies have evaluated the association between the rs2187668 polymorphism in the human leucocyte antigen (HLA) complex class II HLA-DQ a-chain 1 (HLA-DQA1) gene and idiopathic membranous nephropathy (iMN) risk, which provided new insight into potential new targets for the treatment of iMN. However, this relationship remains inconclusive. Our aim was to evaluate the relationship between this polymorphism and iMN susceptibility by performing a meta-analysis.Methods:Articles were identified in the PubMed, Google Scholar, EMBASE, Cochran Library databases. Meta-analyses were performed for rs2187668 allele frequency, genotypes, and the association with iMN susceptibility. Subgroup analyses, publication bias and sensitivity analyses were also conducted.Results:11 eligible studies (3209 cases and 7358 controls) from 7 articles were included. Statistical analyses were carried out using Stata 12.0, combining data from all the relevant studies. The pooled odds ratios (ORs) regarding the association between the HLA-DQA1 rs2187668 polymorphism and iMN risk were statistically significant [A vs G: OR = 3.34, 95% confidence interval (CI) = 2.70–4.13; AA vs GA + GG: OR = 8.69, 95% CI = 6.64–11.36; GG vs GA + AA: OR = 0.25, 95% CI = 0.19–0.33;AA vs GG: OR = 12.61, 95% CI = 8.02–19.81; GA vs GG: OR = 3.45, 95% CI = 2.79–4.25].Conclusions:Our pooled analysis showed a significant association between rs2187668—(A) allele and iMN susceptibility, and the intervention of this mutation might bring new therapeutic strategy for iMN. However, further studies should be performed to confirm this finding.

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Genetic susceptibility to idiopathic membranous nephropathy in high-prevalence Area, Taiwan

Cited by 14 publications

References 56 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

Toll-Like Receptor as a Potential Biomarker in Renal Diseases

Association between the HLA-DQA1 rs2187668 polymorphism and risk of idiopathic membranous nephropathy

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