Evidence map›Paper›PMID 26367486›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2015

miR-101a and miR-30b contribute to inflammatory cytokine-mediated β-cell dysfunction.

Ying Zheng, Zhen Wang, Yiting Tu, Hongwei Shen, Zhijie Dai, Jian Lin, Zhiguang Zhou

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  5. The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024
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  8. Genetics of diabetes.World journal of diabetes · 2023
    Review
  9. Review
  10. Glycemia-Induced miRNA Changes: A Review.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Insights from Dysregulated mRNA Expression Profile ofJournal of immunology research · 2022
    Article
  16. Article
  17. Review
  18. Epigenetics, microRNA and Metabolic Syndrome: A Comprehensive Review.International journal of molecular sciences · 2021
    Review
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Ying ZhengCenter for Medical Research, 2nd Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhen WangDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, China.
Yiting TuDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, China.
Hongwei ShenCenter for Medical Research, 2nd Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhijie DaiDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, China.
Jian LinDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, China.
Zhiguang ZhouDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory cytokines have a critical role in the progressive deterioration of pancreatic β-cell function and development of type 1 diabetes. Prolonged exposure of β-cells to inflammatory cytokines results in gene expression modifications, leading to loss of β-cell function. MicroRNAs (miRNAs) are small non-coding RNAs acting as key regulators of gene expression. Here, we demonstrate that miR-101a and miR-30b are key players in cytokine-mediated β-cell dysfunction. We found that IL-1β induces an increase in miR-101a and miR-30b in MIN6 cells, and that the two miRNAs participate in β-cell dysfunction, including decreased insulin content, gene expression, and increased β-cell death. miR-101a and miR-30b reduce proinsulin expression and insulin content by directly targeting the transcriptional factor Neurod1. In addition, β-cell apoptosis mediated by miR-101a and miR-30b is associated with diminished expression level of the antiapoptotic protein Bcl2. Moreover, we show that miR-101a causes an impairment in glucose-induced insulin secretion by decreasing the expression of the transcription factor Onecut2. Taken together, our findings suggest that changes in the levels of miR-101a and miR-30b contribute to cytokine-mediated β-cell dysfunction occurring during the development and progression of type 1 diabetes.

Indexed as

AnimalsApoptosisBasic Helix-Loop-Helix ProteinsCytokinesDiabetes Mellitus, Type 1HEK293 CellsHomeodomain ProteinsHumansInsulinInsulin-Secreting CellsMicroRNAsProto-Oncogene Proteins c-bcl-2Transcription FactorsBasic Helix-Loop-Helix ProteinsCytokinesHomeodomain ProteinsInsulinMicroRNAsMIRN101 microRNA, humanMIRN30b microRNA, humanNEUROD1 protein, humanONECUT2 protein, humanProto-Oncogene Proteins c-bcl-2Transcription Factors

Identifiers

PMID26367486
OpenAlexW2349396839

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.