Evidence map›Paper›PMID 22911870›Full record

ArticlePloS one2012

Periostin facilitates skin sclerosis via PI3K/Akt dependent mechanism in a mouse model of scleroderma.

Lingli Yang, Satoshi Serada, Minoru Fujimoto, Mika Terao, Yorihisa Kotobuki, Shun Kitaba, Saki Matsui, Akira Kudo, Tetsuji Naka, Hiroyuki Murota and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
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  4. Animal cells and systems · 2024
    Article
  5. The Unknown Role of Periostin in Psoriatic Epidermal Hyperplasia.International journal of molecular sciences · 2023
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  13. Periostin: an emerging activator of multiple signaling pathways.Journal of cell communication and signaling · 2022
    Review
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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 3 institutions in 1 country.

Lingli YangDepartment of Dermatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Satoshi Serada
Minoru Fujimoto
Mika Terao
Yorihisa Kotobuki
Shun Kitaba
Saki Matsui
Akira Kudo
Tetsuji Naka
Hiroyuki Murota
Ichiro Katayama
Osaka University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPTokyo Institute of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePeriostin, a novel matricellular protein, is recently reported to play a crucial role in tissue remodeling and is highly expressed under fibrotic conditions. This study was undertaken to assess the role of periostin in scleroderma.

methodsUsing skin from patients and healthy donors, the expression of periostin was assessed by immunohistochemistry and immunoblotting analyses. Furthermore, we investigated periostin(-/-) (PN(-/-)) and wild-type (WT) mice to elucidate the role of periostin in scleroderma. To induce murine cutaneous sclerosis, mice were subcutaneously injected with bleomycin, while untreated control groups were injected with phosphate-buffered saline. Bleomycin-induced fibrotic changes were compared in PN(-/-) and WT mice by histological analysis as well as by measurements of profibrotic cytokine and extracellular matrix protein expression levels in vivo and in vitro. To determine the downstream pathway involved in periostin signaling, receptor neutralizing antibody and signal transduction inhibitors were used in vitro.

resultsElevated expression of periostin was observed in the lesional skin of patients with scleroderma compared with healthy donors. Although WT mice showed marked cutaneous sclerosis with increased expression of periostin and increased numbers of myofibroblasts after bleomycin treatment, PN(-/-) mice showed resistance to these changes. In vitro, dermal fibroblasts from PN(-/-) mice showed reduced transcript expression of alpha smooth actin and procollagen type-I alpha 1 (Col1α1) induced by transforming growth factor beta 1 (TGFβ1). Furthermore, recombinant mouse periostin directly induced Col1α1 expression in vitro, and this effect was inhibited by blocking the αv integrin-mediated PI3K/Akt signaling either with anti-αv functional blocking antibody or with the PI3K/Akt kinase inhibitor LY294002.

conclusionPeriostin plays an essential role in the pathogenesis of Bleomycin-induced scleroderma in mice. Periostin may represent a potential therapeutic target for human scleroderma.

Indexed as

AdultAgedAnimalsBleomycinCell Adhesion MoleculesCell DifferentiationCollagen Type ICollagen Type I, alpha 1 ChainDisease Models, AnimalExtracellular Matrix ProteinsFemaleFibrosisGene Knockout TechniquesHumansIntegrin alphaVMaleBleomycinCell Adhesion MoleculesCol1a1 protein, mouseCollagen Type ICollagen Type I, alpha 1 ChainExtracellular Matrix ProteinsIntegrin alphaVPhosphatidylinositol 3-KinasesPostn protein, mouseProto-Oncogene Proteins c-aktTransforming Growth Factor beta1

Identifiers

PMID22911870
PMCPMC3404023
OpenAlexW1980798498

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.