Evidence map›Paper›PMID 29666468›Full record

ArticleCell death and differentiation2018

A novel endogenous damage signal, glycyl tRNA synthetase, activates multiple beneficial functions of mesenchymal stem cells.

Se-Ra Park, Hyun-Jin Kim, Se-Ran Yang, Chan Hum Park, Hwa-Yong Lee, In-Sun Hong

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Review
  11. Tryptophanyl-tRNA Synthetase as a Potential Therapeutic Target.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Sonic Hedgehog as a Regulator of Endometrial Mesenchymal Stem/Stromal Cell Activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  15. Article
  16. Article
  17. 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 4 institutions in 1 country.

Se-Ra ParkLaboratory of Stem Cell Research, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea.
Hyun-Jin KimLaboratory of Stem Cell Research, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea.
Se-Ran YangDepartment of Thoracic and Cardiovascular Surgery, Kangwon National University, Chuncheon, South Korea.
Chan Hum ParkDepartment of Otolaryngology-Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, South Korea.
Hwa-Yong LeeDepartment of Biomedical Science, Jungwon University, 85 Goesan-eup, Munmu-ro, Goesan-gun, 367-700, Republic of Korea. hylee@jwu.ac.kr.
In-Sun HongLaboratory of Stem Cell Research, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea. hongstem@gachon.ac.kr.
Gachon University · KRHallym University · KRJungwon University · KRKangwon National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During tissue repair, the injury site releases various bioactive molecules as damage signals to actively recruit stem cells to the damaged region. Despite convincing evidence that mesenchymal stem cells (MSCs) can sense damage signals and promote repair processes, the identity of these signals and how these signals regulate stem cell-mediated tissue repair remain unknown. Glycyl tRNA synthetase (GRS) is a ubiquitously expressed enzyme that catalyzes the first step of protein synthesis in all organisms. In addition to this canonical function, we identified for the first time that GRS is released by damaged tissues or cells in response to various injury signals and may function as a damage signal that activates the proliferative, differentiation, and migratory potential of MSCs, possibly through its identified receptor, cadherin-6 (CDH-6). Binding between GRS and CDH-6 activates survival signals, such as those of the PI3K/Akt and/or FAK/ERK1/2 pathways. More importantly, we also found that MSCs stimulated with GRS show significantly improved homing and differentiation potential and subsequent in vivo therapeutic effects, in a liver fibrosis animal model. Collectively, our findings provide compelling evidence for a novel function of GRS in enhancing the multiple beneficial functions of stem cells via a non-canonical mechanism as a damage signal.

Indexed as

Adipose TissueCadherinsCarbon TetrachlorideCell DifferentiationCell MovementCells, CulturedCell SurvivalFocal Adhesion Kinase 1Glycine-tRNA LigaseHumansLiver Failure, AcuteMAP Kinase Signaling SystemMatrix Metalloproteinase 2Mesenchymal Stem CellsNanog Homeobox ProteinPhosphatidylinositol 3-KinasesCadherinsCarbon TetrachlorideFocal Adhesion Kinase 1Glycine-tRNA LigaseK cadherinMatrix Metalloproteinase 2Nanog Homeobox ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID29666468
PMCPMC6219488
OpenAlexW2802920903

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.