Evidence map›Paper›PMID 33564883›Full record

ArticleEndocrinology2021

microRNA-483 Protects Pancreatic β-Cells by Targeting ALDH1A3.

Zhihong Wang, Ramkumar Mohan, Xinqian Chen, Katy Matson, Jackson Waugh, Yiping Mao, Shungang Zhang, Wanzhen Li, Xiaohu Tang, Leslie S Satin and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Zhihong WangDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Ramkumar MohanDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Xinqian ChenDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Katy MatsonDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Jackson WaughDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Yiping MaoDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Shungang ZhangDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Wanzhen LiDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Xiaohu TangDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Leslie S SatinDepartment of Pharmacology, Brehm Center for Diabetes, University of Michigan, Ann Arbor, MI, USA.
Xiaoqing TangDepartment of Biological Sciences, Michigan Technological University, Houghton, MI, USA.
Michigan Technological University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
METABOLICALLY-COUPLED ION CHANNEL INTERACTIONS IN ISLETSR01DK046409 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SATIN, LESLIE S. · 1994 to 2023
$9.1M
Role of miR-483 in Pancreatic Alpha and Beta CellsR15DK103197 · NIDDK · MICHIGAN TECHNOLOGICAL UNIVERSITY · PI TANG, XIAOQING · 2015 to 2015
$422k
Exploiting synthetic lethality of cysteine addiction to target breast cancerR15CA246336 · NCI · MICHIGAN TECHNOLOGICAL UNIVERSITY · PI TANG, XIAOHU · 2020 to 2020
$413k
NCI NIH HHS R15 CA246336NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK046409NIDDK NIH HHS R15 DK103197
6 · The paper itself

Abstract

Pancreatic β-cell dysfunction is central to the development and progression of type 2 diabetes. Dysregulation of microRNAs (miRNAs) has been associated with pancreatic islet dysfunction in type 2 diabetes. Previous study has shown that miR-483 is expressed relatively higher in β-cells than in α-cells. To explore the physiological function of miR-483, we generated a β-cell-specific knockout mouse model of miR-483. Loss of miR-483 enhances high-fat diet-induced hyperglycemia and glucose intolerance by the attenuation of diet-induced insulin release. Intriguingly, mice with miR-483 deletion exhibited loss of β-cell features, as indicated by elevated expression of aldehyde dehydrogenase family 1, subfamily A3 (Aldh1a3), a marker of β-cell dedifferentiation. Moreover, Aldh1a3 was validated as a direct target of miR-483 and overexpression of miR-483 repressed Aldh1a3 expression. Genetic ablation of miR-483 also induced alterations in blood lipid profile. Collectively, these data suggest that miR-483 is critical in protecting β-cell function by repressing the β-cell disallowed gene Aldh1a3. The dysregulated miR-483 may impair insulin secretion and initiate β-cell dedifferentiation during the development of type 2 diabetes.

Indexed as

AnimalsCell DifferentiationDiabetes Mellitus, Type 2HumansInsulinInsulin-Secreting CellsInsulin SecretionMaleMiceMice, KnockoutMicroRNAsRetinal DehydrogenaseInsulinMicroRNAsMirn483 microRNA, mouseretinaldehyde dehydrogenase 3, mouseRetinal DehydrogenaseAldh1a3disallowed geneinsulin secretionmiR-483miRNAs

Identifiers

PMID33564883
PMCPMC7951052
OpenAlexW3128149486

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.