Evidence map›Paper›PMID 30814673›Full record

ArticleGene therapy2019

ILK promotes survival and self-renewal of hypoxic MSCs via the activation of lncTCF7-Wnt pathway induced by IL-6/STAT3 signaling.

Qing Mao, Xiu-Lin Liang, Yu-Fu Wu, Yi-Heng Pang, Xiao-Jun Zhao, Yong-Xiang Lu

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
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

6 authors at 3 institutions in 1 country.

Qing MaoDepartment of Cardiology, Nanjing Lishui People's Hospital, Zhongda Hospital Lishui Branch, Southeast University, 211200, Nanning, P.R. China. maoqing371@163.com.
Xiu-Lin LiangDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, 530007, Nanning, P.R. China.
Yu-Fu WuDepartment of Cardiology, The Guangxi Zhuang Autonomous Region Brain Hospital, 545005, Liuzhou, P.R. China.
Yi-Heng PangDepartment of Cardiology, The Second Affiliated Hospital of Guangxi Medical University, 530007, Nanning, P.R. China.
Xiao-Jun ZhaoDepartment of Cardiology, The Second Affiliated Hospital of Guangxi Medical University, 530007, Nanning, P.R. China.
Yong-Xiang LuDepartment of Cardiology, The Second Affiliated Hospital of Guangxi Medical University, 530007, Nanning, P.R. China.
Guangxi Medical University · CNGuangxi Zhuang Autonomous Region Brain Hospital · CNLishui City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) have been applied in treating various diseases including myocardial infarction (MI) and achieved a bit of success; however, the decreased survival rate of MSCs after transplantation greatly limited the efficacy for cell therapy. How to improve the MSC survival rate in stem cell transplantation has undoubtedly become urgent and genetic engineering may be an ideal and feasible way. In this study, we explored the effects on MSCs survival and self-renewal by overexpression of integrin-linked kinase (ILK) in MSCs under hypoxic stimulation and aimed to reveal the molecular mechanisms from the point of paracrine function of MSCs. We first found that overexpression of ILK induced the expression and secretion of IL-6 increased significantly in MSCs under hypoxic stimulation, and the survival and self-renewal of MSCs exposed to hypoxia were enhanced after ILK overexpression. Then the activation of JAK2/STAT3 signaling was detected because of the increased IL-6, and an lncRNA, named lncTCF7, was upregulated remarkably, promoting the activation of Wnt pathway that was required for keeping cell viability and stemness of MSCs. Moreover, we further verified that inhibition of STAT3 signaling by WP1066 and silencing lncTCF7 expression eliminated the protective effects of ILK overexpression on cell survival and self-renewal of MSCs under hypoxic sitmulation. In conclusion, our results uncovered a novel function of ILK to promote MSC survival and self-renewal, suggesting more application potentials of MSC cell therapy on MI.

Indexed as

Cell ProliferationWnt Signaling PathwayAnimalsCell HypoxiaCells, CulturedHEK293 CellsHumansInterleukin-6Janus Kinase 2MaleMesenchymal Stem CellsProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyRNA, Long NoncodingScaffold Protein ILKInterleukin-6Janus Kinase 2Protein Serine-Threonine KinasesRNA, Long NoncodingScaffold Protein ILKSTAT3 Transcription Factor

Identifiers

PMID30814673
OpenAlexW2916864207

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.