Evidence map›Paper›PMID 35035844›Full record

ArticleJournal of healthcare engineering2022

hMSCs Migrate under the Chemotaxis of CXCL-13 and Enhance Islet B Cell Activity through p-AKT Signaling Pathway in High-Glucose Environment.

Yongtao Li, Wenshan Bian, Yang Jiang, Danyang Liu, Lei Shen

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of healthcare engineering, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yongtao LiDepartment of Anatomy, Basic Medical College, Qiqihar Medical University, Qiqihar 161006, Heilongjiang, China.ORCID 0000-0003-2573-701X
Wenshan BianDepartment of Anatomy, Basic Medical College, Qiqihar Medical University, Qiqihar 161006, Heilongjiang, China.ORCID 0000-0002-1384-0418
Yang JiangDepartment of Anatomy, Basic Medical College, Qiqihar Medical University, Qiqihar 161006, Heilongjiang, China.ORCID 0000-0002-8899-9239
Danyang LiuDepartment of Histology and Embryolog, Basic Medical College, Qiqihar Medical University, Qiqihar 161006, Heilongjiang, China.ORCID 0000-0002-5508-6724
Lei ShenDepartment of Anatomy, Basic Medical College, Qiqihar Medical University, Qiqihar 161006, Heilongjiang, China.ORCID 0000-0002-5606-0534
Qiqihar Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a common clinical chronic disease, the incidence of diabetes is increasing year by year. According to the latest statistics from the International Diabetes Federation, as of 2019, the global prevalence of diabetes has reached 8.3%. This study aims to investigate the effect of CXCL-13 on the migration ability of human mesenchymal stem cells (hMSCs) and to clarify the specific molecular mechanism of the protective effect of hMSCs on islet B cells. The hMSCs were cultured in high-glucose environment, and the effect of CXCL-13 on the migration ability of hMSCs was determined by Transwell experiment. After coculture of hMSCs and islet B cells, the activity of cells was detected by CCK8 assay, the expression of Ki-67 in cells was detected by RT-PCR, and the expression of P53 was detected by Western blot to investigate the effect of hMSCs on the proliferation and apoptosis of islet B cells. The effect of hMSCs on the function of islet B cells was determined by glucose stimulated insulin secretion experiment. Transwell experiment results showed that CXCL-13 could promote the migration of hMSCs to islet B cells in high-glucose environment. The results of CCK-8 showed that the cell activity in the coculture group was significantly higher than that of the other groups, and RT-PCR showed that the expression of Ki-67 was significantly increased in the coculture group of hMSCs and islet B cells. The results of Western blot showed that the expression of P53 was significantly decreased in the coculture group, and the glucose stimulated insulin secretion test showed that insulin secretion was significantly increased. It was found that after the inhibition of ATK, cell activity was significantly reduced, and apoptosis was significantly increased. Meanwhile, the expression of Ki-67 was inhibited, the expression of P-53 was significantly increased, and insulin secretion was significantly reduced. To sum up, in a high-glucose environment, CXCL-13 effectively promoted the migration of hMSCs, and hMSCs protected the activity and function of islet B cells through Akt signaling pathway.

Indexed as

Diabetes MellitusMesenchymal Stem CellsChemokine CXCL13ChemotaxisGlucoseHumansInsulinKi-67 AntigenProto-Oncogene Proteins c-aktSignal TransductionTumor Suppressor Protein p53Chemokine CXCL13CXCL13 protein, humanGlucoseInsulinKi-67 AntigenProto-Oncogene Proteins c-aktTumor Suppressor Protein p53

Identifiers

PMID35035844
PMCPMC8759880
OpenAlexW4205172324

What OpenQuestion holds

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LicenceCC BY
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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.