Evidence mapPaperPMID 32009808Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2019

Cdc42 Promotes ADSC-Derived IPC Induction, Proliferation, And Insulin Secretion Via Wnt/β-Catenin Signaling.

Xing-Hua Xiao, Qi-Yuan Huang, Xian-Ling Qian, Jing Duan, Xue-Qiao Jiao, Long-Yuan Wu, Qing-Yun Huang, Jun Li, Xing-Ning Lai, Yu-Bo Shi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 24 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Xing-Hua Xiao *Department of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Qi-Yuan Huang *Department of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.ORCID 0000-0003-0731-3336
Xian-Ling Qian *Department of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.ORCID 0000-0001-5366-4976
Jing DuanDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Xue-Qiao JiaoDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Long-Yuan WuDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.ORCID 0000-0002-6751-8715
Qing-Yun HuangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Jun LiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Xing-Ning LaiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Yu-Bo ShiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.
Li-Xia XiongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang 330006, People's Republic of China.ORCID 0000-0003-3769-2496
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeType 1 diabetes mellitus (T1DM) is characterized by irreversible islet β cell destruction. Accumulative evidence indicated that Cdc42 and Wnt/β-catenin signaling both play a critical role in the pathogenesis and development of T1DM. Further, bio-molecular mechanisms in adipose-derived mesenchymal stem cells (ADSCs)-derived insulin-producing cells (IPCs) remain largely unknown. Our aim was to investigate the underlying mechanism of Cdc42/Wnt/β-catenin pathway in ADSC-derived IPCs, which may provide new insights into the therapeutic strategy for T1DM patients.

methodsADSC induction was accomplished with DMSO under high-glucose condition. ML141 (Cdc42 inhibitor) and Wnt-3a (Wnt signaling activator) were administered to ADSCs from day 2 until the induction finished. Morphological changes were determined by an inverted microscope. Dithizone staining was employed to evaluate the induction of ADSC-derived IPCs. qPCR and Western blotting were employed to measure the mRNA and protein expression level of islet cell development-related genes and Wnt signaling-related genes. The proliferation ability of ADSC-derived IPCs was also detected with a cell counting kit (CCK) assay. The expression and secretion of Insulin were detected with immunofluorescence test and enzyme-linked immunosorbent assay (ELISA) respectively.

resultsDuring induction, morphological characters of ADSCs changed into spindle and round shape, and formed islet-line cell clusters, with brown dithizone-stained cytoplasm. Expression levels of islet cell development-related genes were up-regulated in ADSC-derived IPCs. Wnt-3a promoted Wnt signaling markers and islet cell development-related gene expression at mRNA and protein levels, while ML141 played a negative effect. Wnt-3a promoted ADSC-derived IPC proliferation and glucose-stimulated insulin secretion (GSIS), while ML141 played a negative effect.

conclusionOur research demonstrated that DMSO and high-glucose condition can induce ADSCs into IPCs, and Wnt signaling promotes the induction. Cdc42 may promote IPC induction, IPC proliferation and insulin secretion via Wnt/β-catenin pathway, meaning that Cdc42 may be regarded as a potential target in the treatment of T1DM.

Indexed as

ADSCsCdc42insulinIPCsML141Wnt signaling

Identifiers

PMID32009808
PMCPMC6859340
OpenAlexW2985609652

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.