Evidence map›Paper›PMID 31368666›Full record

ArticleJournal of diabetes investigation2020

Wingless-type MMTV integration site family member 5a is a key inhibitor of islet stellate cells activation.

Wei Xu, HouFa Geng, Jun Liang, Ying Liu, Qian Lv, Jie Wang, Rui Li, Xiu Li Wang, Xui Kui Liu, Peter M Jones and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2020. 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
1.1field-weighted citation impact, top 22% 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, 9 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 3 institutions in 2 countries.

Wei XuDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
HouFa GengDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Jun LiangDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Ying LiuDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Qian LvDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Jie WangDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Rui LiDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Xiu Li WangDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Xui Kui LiuDepartment of Endocrinology, Xuzhou Central Hospital, Xuzhou Institute of Medical Sciences, Affiliated Hospital of Southeast University, Xuzhou, Jiangsu, China.
Peter M JonesDepartment of Diabetes, School of Life Course Sciences, King's College London, Guy's Campus, London, UK.
Zi Lin SunDepartment of Endocrinology, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing, China.ORCID https://orcid.org/0000-0001-5357-5332
Xuzhou Central Hospital · CNKing's College London · GBZhongda Hospital Southeast University · CN

Funding

Natural Science Foundation of Jiangsu Province BK20171171Xuzhou Science and Technology Bureau project KC16SH110
6 · The paper itself

Abstract

AIMS/

introductionType 2 diabetes mellitus is a chronic metabolic disorder characterized by islet β-cell dysfunction, which might result from the activation of islet stellate cells (ISCs). Our recent study showed that a specific population of ISCs is prone to be activated in type 2 diabetes mellitus accompanied by reduced secretion of insulin. The wingless-type MMTV integration site family member 5a (Wnt5a)/frizzled-5 signaling pathway might play an important role in this process. The present study aimed to explore the effects of Wnt5a on the activation of ISCs isolated from db/db mice. MATERIALS AND

methodsISCs were isolated from db/db mice and matched db/m mice. Immunohistochemistry and western blotting analysis were applied for the determination of Wnt5a expression. Exogenous Wnt5a and lentivirus containing the target gene Wnt5a short hairpin ribonucleic acid were used as a molecular intervention. The experiment of transwell and wound healing was used to evaluate the migration of the isolated ISCs.

resultsOur data showed that the expression of Wnt5a and frizzled-5 was decreased in the ISCs isolated from db/db mice compared with db/m mice. Both the exogenous Wnt5a and the overexpression of Wnt5a could inhibit the outgrowth rate of ISCs from islets, and its viability, migration and α smooth muscle actin expression. These changes were associated with the inactivation of the Smad2/3 signaling pathway in a frizzled-5-dependent manner.

conclusionsOur observations revealed a potential role of Wnt5a in preventing ISC activation. The maintenance of quiescent ISCs might be a desirable outcome of therapeutic strategies for diabetes mellitus.

Indexed as

AnimalsApoptosisCells, CulturedFrizzled ReceptorsMaleMice, Inbred C57BLMice, KnockoutPancreatic Stellate CellsSmad2 ProteinSmad3 ProteinWnt-5a ProteinFrizzled ReceptorsFzd5 protein, mouseSmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseWnt-5a ProteinWnt5a protein, mouseIslet stellate cellsType 2 diabetes mellitusWingless-type MMTV integration site family member 5a

Identifiers

PMID31368666
PMCPMC7078096
OpenAlexW2964806026

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.