Evidence map›Paper›PMID 21990361›Full record

ArticleThe Journal of biological chemistry2011

Delayed re-epithelialization in Ppm1a gene-deficient mice is mediated by enhanced activation of Smad2.

Xue Yang, Yan Teng, Ning Hou, Xiongwei Fan, Xuan Cheng, Jun Li, Lijuan Wang, Youliang Wang, Xiushan Wu, Xiao Yang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. The Long Noncoding RNADNA and cell biology · 2022
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  7. Article
  8. Article
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  10. Loss of expression of protein phosphatase magnesium-dependent 1A during kidney injury promotes fibrotic maladaptive repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
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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

10 authors at 4 institutions in 1 country.

Xue YangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China; Model Organism Division, E-institutes of Shanghai Universities, Shanghai JiaoTong University, Shanghai 200025, P.R. China.
Yan TengState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China. Electronic address: tengyan0919@tom.com.
Ning HouState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China.
Xiongwei FanState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China; College of Life Sciences, Hunan Normal University, Changsha 410081, P.R. China.
Xuan ChengState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China.
Jun LiState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China.
Lijuan WangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China.
Youliang WangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China.
Xiushan WuCollege of Life Sciences, Hunan Normal University, Changsha 410081, P.R. China.
Xiao YangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing 100071, P.R. China; Model Organism Division, E-institutes of Shanghai Universities, Shanghai JiaoTong University, Shanghai 200025, P.R. China. Electronic address: yangx@nic.bmi.ac.cn.
Hunan Normal University · CNShanghai Jiao Tong University · CNState Key Laboratory of ProteomicsBeijing Proteome Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein phosphatase magnesium-dependent 1A (PPM1A), a protein serine/threonine phosphatase, controls several signal pathways through cleavage of phosphate from its substrates. However, the in vivo function of Ppm1a in mammals remains unknown. Here we reported that mice lacking Ppm1a developed normally but were impaired in re-epithelialization process during cutaneous wound healing. Specifically, complete or keratinocyte-specific deletion of Ppm1a led to delayed re-epithelialization with reduced keratinocyte migration upon wounding. We showed that this effect was the result of an increase in Smad2/3 phosphorylation in keratinocytes. Keratinocyte-specific Smad2 deficient mice displayed accelerated re-epithelialization with enhanced keratinocyte migration. Importantly, Smad2 and Ppm1a double mutant mice also exhibited accelerated re-epithelialization, demonstrating that the effect of Ppm1a on promoting re-epithelialization is mediated by Smad2 signaling. Furthermore, the decreased expression of specific integrins and matrix metalloproteinases (MMPs) may contribute to the retarded re-epithelialization in Ppm1a mutant mice. These data indicate that Ppm1a, through suppressing Smad2 signaling, plays a critical role in re-epithelialization during wound healing.

Indexed as

AnimalsCell MovementGene DeletionGenotypeIntegrinsKeratinocytesMiceMice, KnockoutMice, TransgenicModels, GeneticMutationPhosphoprotein PhosphatasesProtein Phosphatase 2CSignal TransductionSmad2 ProteinWound HealingIntegrinsPhosphoprotein PhosphatasesPpm1a protein, mouseProtein Phosphatase 2CSmad2 ProteinSmad2 protein, mouse

Identifiers

PMID21990361
PMCPMC3234921
OpenAlexW2067838033

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.