Evidence map›Paper›PMID 33423166›Full record

ArticleMolecular and cellular biochemistry2021

MiR-26a regulated adipogenic differentiation of ADSCs induced by insulin through CDK5/FOXC2 pathway.

Xu-Xiang Zhang, Yu-Ming Wang, Yan-Dan Su, Fan Zuo, Bin Wu, Xin Nian

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 38% 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, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xu-Xiang ZhangDepartment of Endocrinology, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China.
Yu-Ming WangDepartment of Clinical Laboratory, Second Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China.
Yan-Dan SuDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China.
Fan ZuoDepartment of Endocrinology, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China.
Bin WuDepartment of Endocrinology, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China.
Xin NianDepartment of Endocrinology, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, People's Republic of China. nianxinx86@163.com.ORCID http://orcid.org/0000-0001-8106-7191
Kunming Medical University · CN

Funding

Joint Research Found of Yunnan Provincial Science and Technology Department-Kunming Medical University Grant No. 2017FE468-197National Natural Science Foundation of China Grant No. 81660153, No.81660141
6 · The paper itself

Abstract

objectiveObesity is associated with an increased risk of developing insulin resistance and type 2 diabetes, since insulin can induce adipogenic differentiation of human adipose-derived stem cells (ADSCs). MiR-26a was reported to be highly expressed in ADSCs under induction and Forkhead box C2 (FOXC2), as a key substrate of cyclin-dependent kinase 5 (CDK5) could inhibit white adipocyte differentiation, which was mediated by miR-26a. However, the relationship between miR-26a and CDK5/FOXC2 during ADSCs differentiation remains unknown. We want to verify the regulated mechanism of miR-26a/CDK5/FOXC2 axis participating in the adipogenic differentiation of ADSCS.

methodsADSCs were isolated and verified by flow cytometry. Oil Red O staining was performed to assess the capacity for adipogenic differentiation of ADSCs. The proliferation ability of ADSCs was verified by MTT assay. The expression of miR-26a, peroxisome proliferator-activated receptors γ (PPARγ), CDK5, and FOXC2 were tested by qRT-PCR and Western blot, and the relationship between miR-26a and CDK5 was verified by dual-luciferase reporter gene assay.

resultsMiR-26a and PPARγ were upregulated and CDK5 and FOXC2 were downregulated during adipogenic differentiation of ADSCs. Knockdown of miR-26a or overexpression of CDK5 could inhibit adipogenic differentiation of ADSCs induced by insulin. MiR-26a could directly target CDK5 and the effect of miR-26a inhibitor on adipogenic differentiation of ADSCs could be blocked by si-CDK5.

conclusionWe demonstrated that miR-26a regulated insulin-induced adipogenic differentiation of ADSCs by regulating CDK5/FOXC2 pathway, which could provide the key to a comprehensive mechanistic understanding of obesity and type 2 diabetes.

Indexed as

AdipogenesisAdipose TissueAnimalsCell DifferentiationCyclin-Dependent Kinase 5Forkhead Transcription FactorsInsulinMicroRNAsRatsRats, Sprague-DawleySignal TransductionStem CellsCdk5 protein, ratCyclin-Dependent Kinase 5Forkhead Transcription FactorsInsulinmesenchyme fork head 1 proteinMicroRNAsMIRN26 microRNA, ratAdipogenic differentiationADSCsCDK5FOXC2miR-26aPPARγ

Identifiers

PMID33423166
OpenAlexW3118669196

What OpenQuestion holds

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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.