Evidence map›Paper›PMID 26563755›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

Rs12976445 Polymorphism is Associated with Risk of Diabetic Nephropathy Through Modulating Expression of MicroRNA-125 and Interleukin-6R.

Cunjie Li, Ting Lei

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In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
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10citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  9. β-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/β-Catenin Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018
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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Cunjie LiDepartment of Endocrinology, Hanzhong People's Hospital, Hanzhong, Shaanxi, China (mainland).
Ting LeiDepartment of Hematology, Hanzhong People's Hospital, Hanzhong, Shaanxi, China (mainland).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is one of the most significant long-term complications of diabetes mellitus (DM), and it is a primary risk factor for end-stage renal disease. MicroRNAs (miRNAs) play important roles in regulating the expression of genes, including interleukin-6R (IL-6R), which has been reported to be involved in the development of DNDN. The aim of this study was to identify the dysregulation of miRNA and its target responsible for the development of DN in DM. MATERIAL AND

methodsWe collected the kidney tissues from patients with DN (N=36) and control patients (N=28), and performed real-time PCR and Western blot analysis to determine the expression of IL-6R. Computational analysis and luciferase assay were used to identify the miRNA that regulates IL-6R. To explore the association between rs12976445 polymorphism and risk of DN, we enrolled 594 DM patients with (N=282) or without DN (N=312), and studied the association between a variant in miR-125a and risk of DN in DM.

resultsThe expression of IL-6R was barely detected in the control groups, while in the DN group, the IL-6R was clearly detectable. Next, miR-125a was identified as a regulator of IL-6R by using informatics analysis and luciferase assay. A single-nucleotide polymorphism (rs12976445) in pri-miR-125a has been shown to compromise the mature processing of miR-125a, and we showed that the expression levels of miR-125a was comparable between individuals carrying TT and CT, and when combined into 1 group, the miR-125a expression was approximately 3 times lower than in the CC group. We found significant differences regarding rs12976445 genotype distribution between the DN and the control (OR=1.45, 95% C.I.=1.02-2.08, p<0.05) with the possible confounding factors adjusted for by using logistic regression analysis.

conclusionsWe identified miR-125a as a direct regulator of IL-6R, and the genotype of rs12976445 might be a novel predictor of the development of DN in DM.

Indexed as

AdultAgedCase-Control StudiesDiabetic NephropathiesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansKidney Failure, ChronicMaleMicroRNAsMiddle AgedPolymorphism, Single NucleotideReal-Time Polymerase Chain ReactionReceptors, Interleukin-6Risk FactorsIL6R protein, humanMicroRNAsMIRN125 microRNA, humanReceptors, Interleukin-6

Identifiers

PMID26563755
PMCPMC4648103

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.