Evidence map›Paper›PMID 30320384›Full record

ArticleMolecular medicine reports2018

Interleukin‑10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon‑derived stem cells in vitro.

Ganming Deng, Kaiqun Li, Siwei Chen, Peisheng Chen, Haonan Zheng, Bin Yu, Kairui Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 26 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

7 authors at 3 institutions in 1 country.

Ganming DengDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Kaiqun LiDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Siwei ChenDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Peisheng ChenDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Haonan ZhengThe Third Clinical College of Guangzhou Medical University, Guangzhou, Guangdong 510515, P.R. China.
Bin YuDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Kairui ZhangDepartment of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Nanfang Hospital · CNSouthern Medical University · CNThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tendon repair follows a slow course of early inflammatory, proliferative and remodeling phases, which commonly results in the failure and loss of normal biomechanical properties. Previous studies have demonstrated that tendon‑derived stem cells (TDSCs) are vital healing cells and that mRNA expression of anti‑inflammatory cytokine interleukin (IL)‑10 is significantly upregulated at the late inflammatory phase. To explore how IL‑10 may impact tendon healing, the present study investigated the in vitro effects of IL‑10 on TDSCs isolated from rat Achilles tendons. Cellular activities of TDSCs and the expression levels of tendon cell markers were measured treatment with IL‑10 and subsequent performance of wound healing assays, reverse transcription‑quantitative polymerase chain reaction and western blot analyses. The results demonstrated that IL‑10 treatment markedly increased the proliferative capacity of TDSCs. In addition, IL‑10 significantly enhanced cell migration when compared with the control cells. Furthermore, IL‑10 treatment significantly activated the JAK/Stat3 signaling pathway and inhibited the protein expression of tendon cell markers, including scleraxis and tenomodulin. Notably, IL‑10 treatment also reduced the gene expression levels of type 1 collagen, type 3 collagen, lumican and fibromodulin in TDSCs. These findings indicated that IL‑10 enhanced cell proliferation and migration, and inhibited tenogenic differentiation in TDSCs in vitro. Reducing the negative effects whilst enhancing the positive effects of IL‑10 may be a potential therapeutic target in tendon repair.

Indexed as

Cell DifferentiationAnimalsCell CycleCell MovementCell ProliferationCells, CulturedFemaleInterleukin-10Janus KinasesRatsSTAT3 Transcription FactorStem CellsTendonsWound HealingInterleukin-10Janus KinasesSTAT3 Transcription Factorinjuryinterleukin‑10tendontendon‑derived stem cells

Identifiers

PMID30320384
PMCPMC6236255
OpenAlexW2898021340

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.