Evidence map›Paper›PMID 19541844›Full record

ArticleAmerican journal of respiratory cell and molecular biology2010

Conditional overexpression of connective tissue growth factor disrupts postnatal lung development.

Shu Wu, Astrid Platteau, Shaoyi Chen, George McNamara, Jeffrey Whitsett, Eduardo Bancalari

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
  3. Review
  4. Alveologenesis: What Governs Secondary Septa Formation.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Attenuation of miR-17∼92 Cluster in Bronchopulmonary Dysplasia.Annals of the American Thoracic Society · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia.Birth defects research. Part A, Clinical and molecular teratology · 2014
    Review
  18. Article
  19. Article
  20. Mechanisms of bronchopulmonary dysplasia.Journal of cell communication and signaling · 2013
    Article
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

6 authors at 2 institutions in 1 country.

Shu WuDepartment of Pediatrics, Division of Neonatology, University of Miami Miller School of Medicine, Miami, Florida 33101, USA. swu2@med.miami.edu
Astrid Platteau
Shaoyi Chen
George McNamara
Jeffrey Whitsett
Eduardo Bancalari
University of Miami · USCincinnati Children's Hospital Medical Center · US

Funding

CTGF in Normal and Deranged Lung MorphogenesisK08HD046582 · NICHD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WU, SHU · 2005 to 2009
$653k
NICHD NIH HHS K08 HD046582
6 · The paper itself

Abstract

Connective tissue growth factor (CTGF) is a member of an emerging family of immediate-early gene products that coordinates complex biological processes during development, differentiation, and tissue repair. Overexpression of CTGF is associated with mechanical ventilation with high tidal volume and oxygen exposure in newborn lungs. However, the role of CTGF in postnatal lung development and remodeling is not well understood. In the present study, a double-transgenic mouse model was generated with doxycycline-inducible overexpression of CTGF in respiratory epithelial cells. Overexpression of CTGF from Postnatal Days 1-14 resulted in thicker alveolar septa and decreased secondary septal formation. This is correlated with increased myofibroblast differentiation and disorganized elastic fiber deposition in alveolar septa. Overexpression of CTGF also decreased alveolar capillary network formation. There were increased alpha-smooth muscle actin expression and collagen deposition, and dramatic thickening in the peribronchial/peribronchiolar and perivascular regions in the double-transgenic lungs. Furthermore, overexpression of CTGF increased integrin-linked kinase expression, activated its downstream signaling target, Akt, as well as increased mRNA expression of fibronectin. These data demonstrate that overexpression of CTGF disrupts alveologenesis and capillary formation, and induces fibrosis during the critical period of alveolar development. These histologic changes are similar to those observed in lungs of infants with bronchopulmonary dysplasia.

Indexed as

AnimalsAnimals, NewbornApoptosisCapillariesCell DifferentiationCell ProliferationConnective Tissue Growth FactorElastic TissueEpithelial CellsFibroblastsLungMiceMice, Inbred C57BLMice, TransgenicProtein Serine-Threonine KinasesPulmonary AlveoliConnective Tissue Growth FactorProtein Serine-Threonine KinasesScaffold Protein ILK

Identifiers

PMID19541844
PMCPMC2874441
OpenAlexW2131115886

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.