Evidence map›Paper›PMID 16251409›Full record

ArticleThe American journal of pathology2005

Gene expression profiles reveal increased mClca3 (Gob5) expression and mucin production in a murine model of asbestos-induced fibrogenesis.

Tara Sabo-Attwood, Maria Ramos-Nino, Jeffrey Bond, Kelly J Butnor, Nicholas Heintz, Achim D Gruber, Chad Steele, Douglas J Taatjes, Pamela Vacek, Brooke T Mossman

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Comparing the Protection Imparted by Different Fraction Extracts of Garlic (International journal of molecular sciences · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Chronic intermittent hypoxia decreases pulmonary clearance ofAmerican journal of translational research · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 5 institutions in 3 countries.

Tara Sabo-AttwoodDepartment of Pathology, University of Vermont, 89 Beaumont Ave., HSRF 218, Burlington, VT 05405, and the Pediatric Pulmonary Division, Children's Hospital of Pittsburgh, PA, USA.
Maria Ramos-Nino
Jeffrey Bond
Kelly J Butnor
Nicholas Heintz
Achim D Gruber
Chad Steele
Douglas J Taatjes
Pamela Vacek
Brooke T Mossman
University of Vermont · USChildren's Hospital of Pittsburgh · USFreie Universität Berlin · DEInstitute for Medical Informatics and Biostatistics · CHUniversity of Vermont Medical Center · US

Funding

SIGNALING IN EPITHELIAL INJURY, PROLIFERATION &FIBROSISP01HL067004 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MOSSMAN, BROOKE TAYLOR · 2001 to 2005
$7.6M
ENVIRONMENTAL PATHOLOGY TRAINING PROGRAMT32ES007122 · NIEHS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 1985 to 2012
$4.2M
NHLBI NIH HHS HL67004NHLBI NIH HHS P01 HL067004NIEHS NIH HHS T32 ES007122NIEHS NIH HHS T32ES07122
6 · The paper itself

Abstract

To elucidate genes important in development or repair of asbestos-induced lung diseases, gene expression was examined in mice after inhalation of chrysotile asbestos for 3, 9, and 40 days. We identified changes in the expression of genes linked to proliferation (cyclin B2, CDC20, and CDC28 protein kinase regulatory subunit 2), inflammation (CCL9, CCL6, complement component 1, chitinase3-like 3, TNF superfamily member 10, and IL-1B), and matrix remodeling (MMP12, MMP3, integrin alphaX, and cathepsins K, Z, B, and S). The most highly induced gene at all time points was mclca3 (gob5), a putative calcium-activated chloride channel involved in the regulation of mucus production and/or secretion. Using histochemistry, we demonstrated accumulation of mucus and increased mClca3 protein in the bronchiolar epithelium of asbestos-exposed mice at all time points but peaking at 9 days. Cytokine levels (interleukin-1beta, interleukin-4, interleukin-6) in bronchoalveolar lavage fluid also increased at 9 days, suggesting Th2-mediated immunity may play a role in asbestos-induced mucus production. In contrast, levels of cathepsin K, a potent elastase, increased between 3 and 40 days at both the mRNA and protein levels, localizing primarily in CD45-positive leukocytes and interstitial cells. Identification of genes involved in lung injury and remodeling after asbestos exposure could aid in defining mechanisms of airborne particulate-induced disease and in developing therapeutic strategies.

Indexed as

Gene ExpressionGene Expression ProfilingAnimalsAsbestosAsbestosisBronchoalveolar Lavage FluidChloride ChannelsCytokinesDisease Models, AnimalImmunohistochemistryMaleMiceMice, Inbred C57BLMucinsMucoproteinsOligonucleotide Array Sequence AnalysisAsbestosChloride ChannelsClca3a1 protein, mouseCytokinesMucinsMucoproteinsPancreatic ElastaseRNA, Messenger

Identifiers

PMID16251409
PMCPMC1603789
OpenAlexW2019843033

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.