Evidence map›Paper›PMID 26208605›Full record

ArticleInflammation2016

MicroRNA-26a Promotes Regulatory T cells and Suppresses Autoimmune Diabetes in Mice.

Hui Ma, Shoutao Zhang, Doufei Shi, Yanhua Mao, Jianguo Cui

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. The Profiling and Role of miRNAs in Diabetes Mellitus.Journal of diabetes and clinical research · 2019
    Article
  10. Review
  11. Article
  12. Article
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

5 authors at 1 institution in 1 country.

Hui MaDepartment of Geriatrics, Affiliated Hospital of Binzhou Medical University, No.661, Section 2, The Yellow River Road, Binzhou, Shandong, 256603, China. mahui0001@yeah.net.
Shoutao ZhangDepartment of Orthopedics, Affiliated Hospital of Binzhou Medical University, Binzhou, 256603, China.
Doufei ShiDepartment of Geriatrics, Affiliated Hospital of Binzhou Medical University, No.661, Section 2, The Yellow River Road, Binzhou, Shandong, 256603, China.
Yanhua MaoDepartment of Geriatrics, Affiliated Hospital of Binzhou Medical University, No.661, Section 2, The Yellow River Road, Binzhou, Shandong, 256603, China.
Jianguo CuiDepartment of Geriatrics, Affiliated Hospital of Binzhou Medical University, No.661, Section 2, The Yellow River Road, Binzhou, Shandong, 256603, China.
Binzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type-1 diabetes (TID) is an autoimmune disease in which the body's own immune cells attack islet β cells, the cells in the pancreas that produce and release the hormone insulin. Mir-26a has been reported to play functions in cellular differentiation, cell growth, cell apoptosis, and metastasis. However, the role of microRNA-26a (Mir-26a) in autoimmune TID has never been investigated. In our current study, we found that pre-Mir-26a (LV-26a)-treated mice had significantly longer normoglycemic time and lower frequency of autoreactive IFN-γ-producing CD4(+) cells compared with an empty lentiviral vector (LV-Con)-treated non-obese diabetic (NOD) mice. Mir-26a suppresses autoreactive T cells and expands Tregs in vivo and in vitro. Furthermore, in our adoptive transfer study, the groups receiving whole splenocytes and CD25-depleted splenocytes from LV-Con-treated diabetic NOD mice develop diabetes at 3 to 4 weeks of age. In comparison, mice injected with undepleted splenocytes obtained from LV-26a-treated reversal NOD mice develop diabetes after 6-8 weeks. And depletion of CD25(+) cells in the splenocytes of reversed mice abrogates the delay in diabetes onset. In conclusion, Mir-26a suppresses autoimmune diabetes in NOD mice in part through promoted regulatory T cells (Tregs) expression.

Indexed as

Adoptive TransferAnimalsDiabetes Mellitus, Type 1FemaleHyperglycemiaInflammationInterferon-gammaInterleukin-2 Receptor alpha SubunitIslets of LangerhansLymphocyte ActivationMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDMicroRNAsSpleenIl2ra protein, mouseInterferon-gammaInterleukin-2 Receptor alpha SubunitMicroRNAsMirn26 microRNA, mousemicroRNA-26aNOD miceregulatory T cellstype-1 diabetes

Identifiers

PMID26208605
OpenAlexW1435450345

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.