Evidence map›Paper›PMID 27897224›Full record

ArticleScientific reports2016

TGF-β1 Induces Polypyrimidine Tract-Binding Protein to Alter Fibroblasts Proliferation and Fibronectin Deposition in Keloid.

Hu Jiao, Ping Dong, Li Yan, Zhigang Yang, Xiaoyan Lv, Qiuchen Li, Xianlei Zong, Jincai Fan, Xin Fu, Xia Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  9. PAI-1 mediates TGF-β1-induced myofibroblast activation in tenocytes via mTOR signaling.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2023
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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 2 institutions in 1 country.

Hu JiaoResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Ping DongResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Li YanResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Zhigang YangResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Xiaoyan LvResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Qiuchen LiResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Xianlei ZongScar Plastic Department of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Jincai FanScar Plastic Department of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Xin FuResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Xia LiuResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Ran XiaoResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences &Peking Union Medical College, Beijing, P.R. China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human dermal fibrotic disease keloid has been a clinical challenge because of its tumour-like growth and the lack of effective therapy. Dysregulated alternative splicing events have been demonstrated in tumours and fibrosis. In the current study, for the first time, it was demonstrated that the splicing regulator polypyrimidine tract-binding protein (PTB), which plays a pivotal role in tumour proliferation, invasion and metastasis, is overexpressed in keloid tissues and fibroblasts. Additionally, TGF-β1 upregulated the expressions of PTB and its upstream regulator, C-MYC, in keloid fibroblasts. Furthermore, we suppressed PTB using siRNA in keloid fibroblasts and in a keloid xenograft nude mouse model. PTB knockdown significantly slowed the proliferation of keloid fibroblasts and accelerated the regression of transplanted keloid tissues, which was accompanied by a shift in the alternative splicing of USP5 and RTN4. Moreover, when PTB was suppressed, there was a reduction in excessive deposition of FN1 and COL3A1 in transplanted keloid tissues. However, only FN1 was downregulated in keloid fibroblasts that were cultured in media supplemented with TGF-β1. Our study provides evidence for the role of PTB in keloid pathophysiology and offers a novel therapeutic target for keloids. Most importantly, the role TGF-β1 regulation of PTB may provide new insights into the mechanisms underlying inflammatory cytokine-induced fibrosis.

Indexed as

Cell ProliferationAnimalsCytokinesFemaleFibroblastsFibronectinsHeterograftsHumansKeloidMaleMiceMice, NudePolypyrimidine Tract-Binding ProteinTransforming Growth Factor beta1CytokinesFibronectinsFN1 protein, humanPolypyrimidine Tract-Binding ProteinTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID27897224
PMCPMC5126665
OpenAlexW2558011421

What OpenQuestion holds

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LicenceCC BY
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.