Evidence map›Paper›PMID 18188456›Full record

ArticleThe Journal of clinical investigation2008

Pin1 regulates TGF-beta1 production by activated human and murine eosinophils and contributes to allergic lung fibrosis.

Zhong-Jian Shen, Stephane Esnault, Louis A Rosenthal, Renee J Szakaly, Ronald L Sorkness, Pamela R Westmark, Matyas Sandor, James S Malter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
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  5. The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024
    Review
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  7. Article
  8. Article
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  13. Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020
    Review
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  17. 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

8 authors at 3 institutions in 1 country.

Zhong-Jian ShenWaisman Center for Developmental Disabilities, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53705, USA.
Stephane Esnault
Louis A Rosenthal
Renee J Szakaly
Ronald L Sorkness
Pamela R Westmark
Matyas Sandor
James S Malter
Emory University Hospital · USNew York State Office for People With Developmental Disabilities · USUniversity of Wisconsin–Madison · US

Funding

WISCONSIN CENTER ON MENTAL RETARDATION: CORE SUPPORTP30HD003352 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI DAVIDSON, RICHARD J · 1985 to 2015
$25.2M
Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
SCOR--CELLULAR AND MOLECULAR MECHANISMS OF ASTHMAP50HL056396 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 1997 to 2006
$13.8M
NHLBI NIH HHS P01 HL088594NHLBI NIH HHS P50 HL056396NHLBI NIH HHS P50HL56396NICHD NIH HHS P30 HD003352NICHD NIH HHS P30HD03352
6 · The paper itself

Abstract

Eosinophilic inflammation is a cornerstone of chronic asthma that often culminates in subepithelial fibrosis with variable airway obstruction. Pulmonary eosinophils (Eos) are a predominant source of TGF-beta1, which drives fibroblast proliferation and extracellular matrix deposition. We investigated the regulation of TGF-beta1 and show here that the peptidyl-prolyl isomerase (PPIase) Pin1 promoted the stability of TGF-beta1 mRNA in human Eos. In addition, Pin1 regulated cytokine production by both in vitro and in vivo activated human Eos. We found that Pin1 interacted with both PKC-alpha and protein phosphatase 2A, which together control Pin1 isomerase activity. Pharmacologic blockade of Pin1 in a rat asthma model selectively reduced eosinophilic pulmonary inflammation, TGF-beta1 and collagen expression, and airway remodeling. Furthermore, chronically challenged Pin1(-/-) mice showed reduced peribronchiolar collagen deposition compared with wild-type controls. These data suggest that pharmacologic suppression of Pin1 may be a novel therapeutic option to prevent airway fibrosis in individuals with chronic asthma.

Indexed as

AllergensAnimalsAntigens, SurfaceAsthmaBronchiCollagenELAV-Like Protein 1ELAV ProteinsEosinophilsHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HumansMiceMice, Mutant StrainsNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomeraseAllergensAntigens, SurfaceCollagenELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanHnrnpd protein, ratHnrpd protein, mouseNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePIN1 protein, humanPin1 protein, mouseProtein Kinase C-alphaProtein Phosphatase 2RNA-Binding ProteinsRNA, MessengerTransforming Growth Factor beta1

Identifiers

PMID18188456
PMCPMC2176187
OpenAlexW2158376596

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.