Evidence map›Paper›PMID 19411308›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009

Pleural mesothelial cell transformation into myofibroblasts and haptotactic migration in response to TGF-beta1 in vitro.

Najmunnisa Nasreen, Kamal A Mohammed, Kamal K Mubarak, Maher A Baz, Olufemi A Akindipe, Sebastian Fernandez-Bussy, Veena B Antony

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

73 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. A Developmental Roadmap Toward Abdominal Adhesions Prevention Technologies.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2025
    Review
  7. Article
  8. Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  9. Article
  10. Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  11. Myocardin regulates fibronectin expression and secretion from human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  12. Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Regulation of Mesothelial Cell Fate during Development and Human Diseases.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Najmunnisa NasreenDivision of Pulmonary and Critical Care Medicine, Department of Medicine, College of Medicine, University of Florida, Gainesville, Florida, USA. nnasreen@medicine.ufl.edu
Kamal A Mohammed
Kamal K Mubarak
Maher A Baz
Olufemi A Akindipe
Sebastian Fernandez-Bussy
Veena B Antony
University of Florida · US

Funding

HIV, Alcohol and TB PleurisyR21AA014796 · NIAAA · UNIVERSITY OF FLORIDA · PI ANTONY, VEENA B · 2004 to 2006
$1.0M
NIAAA NIH HHS R21-AA-014796
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology characterized by the development of subpleural foci of myofibroblasts that contribute to the exuberant fibrosis noted in the pulmonary parenchyma. Pleural mesothelial cells (PMC) are metabolically dynamic cells that cover the lung and chest wall as a monolayer and are in intimate proximity to the underlying lung parenchyma. The precise role of PMC in the pathogenesis of pulmonary parenchymal fibrosis remains to be identified. Transforming growth factor (TGF)-beta1, a cytokine known for its capacity to induce proliferative and transformative changes in lung cells, is found in significantly higher quantities in the lungs of patients with IPF. High levels of TGF-beta1 in the subpleural milieu may play a key role in the transition of normal PMC to myofibroblasts. Here we demonstrate that PMC activated by TGF-beta1 undergo epithelial-mesenchymal transition (EMT) and respond with haptotactic migration to a gradient of TGF-beta1 and that the transition of PMC to myofibroblasts is dependent on smad-2 signaling. The EMT of PMC was marked by upregulation of alpha-smooth muscle actin (alpha-SMA), fibroblast specific protein-1 (FSP-1), and collagen type I expression. Cytokeratin-8 and E-cadherin expression decreased whereas vimentin remained unchanged over time in transforming PMC. Knockdown of smad-2 gene by silencing small interfering RNA significantly suppressed the transition of PMC to myofibroblasts and significantly inhibited the PMC haptotaxis. We conclude that PMC undergo EMT when exposed to TGF-beta1, involving smad-2 signaling, and PMC may be a possible source of myofibroblasts in IPF.

Indexed as

BiomarkersCadherinsCell Line, TransformedCell MovementCollagen Type ICytoskeletonEpithelial CellsFibroblastsGene SilencingHumansMesodermOrgan SpecificityPhenotypePhosphorylationPleuraRNA, Small InterferingBiomarkersCadherinsCollagen Type IRNA, Small InterferingSmad2 ProteinSMAD2 protein, humanSmad4 ProteinSMAD4 protein, humanTransforming Growth Factor beta1

Identifiers

PMID19411308
PMCPMC2711818
OpenAlexW2116871724

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.