Evidence map›Paper›PMID 33324395›Full record

ArticleFrontiers in immunology2020

microRNA-630 Regulates Underglycosylated IgA1 Production in the Tonsils by Targeting TLR4 in IgA Nephropathy.

Chan Liu, Mu-Yao Ye, Wen-Zhe Yan, Xiao-Fei Peng, Li-Yu He, You-Ming Peng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. IgA nephropathy: gut microbiome regulates the production of hypoglycosilated IgA1 via the TLR4 signaling pathway.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  8. Article
  9. Review
  10. Article
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  12. Cytokines and Production of AberrantlyJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Chan LiuInternational Medical Department, The Second Xiangya Hospital, Central South University, Changsha, China.
Mu-Yao YeDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, China.
Wen-Zhe YanDepartment of Hematology, The Second Xiangya Hospital, Central South University, Changsha, China.
Xiao-Fei PengDepartment of Rheumatology and Immunology, The Second Xiangya Hospital, Central South University, Changsha, China.
Li-Yu HeDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, China.
You-Ming PengDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, China.
Second Xiangya Hospital of Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the most common primary glomerular disease. The characteristic pathology involves immune complexes formed by the deposition of IgA1 and underglycosylated IgA1 aggregates in the mesangial area, which may be accompanied by the deposition of IgG and/or IgM and complement components. However, the molecular mechanisms of IgAN remain unclear. In the present study, microarray analysis showed that the expression of microRNA-630 (miR-630) was significantly reduced in palatal tonsils from IgAN patients compared with chronic tonsillitis. Additionally, bioinformatic analysis showed that Toll-like receptor 4 (TLR4) was the predicted target gene of miR-630 and was regulated by miR-630. When miR-630 was overexpressed in palatal tonsil mononuclear cells from IgAN patients, the expression of TLR4 was reduced and the content of IgA1 in the cell culture supernatant was decreased, and the level of galactosylation in the IgA1 hinge region was increased. Moreover, immunohistochemical analysis showed that the expression of TLR4 in IgAN patients was significantly increased. After knocking down the expression of TLR4, both the concentration of IgA1 and the binding force of IgA1 with broad bean lectin were significantly reduced in IgAN. Furthermore, the mechanism study demonstrated that TLR4 might regulate the expression of IL-1β and IL-8 through NF-κB signaling pathway to modulate the concentration of IgA1 and the glycosylation level of IgA1. This interesting finding may offer new insight into the molecular mechanism of IgAN.

Indexed as

AdolescentAdultBiomarkersCells, CulturedChildFemaleGene Knockdown TechniquesGlomerulonephritis, IGAGlycosylationHumansImmunoglobulin AInterleukin-1betaInterleukin-8MaleMicroRNAsNF-kappa BBiomarkersCXCL8 protein, humanIL1B protein, humanImmunoglobulin AInterleukin-1betaInterleukin-8MicroRNAsMIRN630 microRNA, humanNF-kappa BTLR4 protein, humanToll-Like Receptor 4IgA nephropathymicroRNA-630palatal tonsilsTLR4underglycosylated IgA1

Identifiers

PMID33324395
PMCPMC7725902
OpenAlexW3106805773

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.