Evidence map›Paper›PMID 16214815›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2006

Constitutive activation of prosurvival signaling in alveolar mesenchymal cells isolated from patients with nonresolving acute respiratory distress syndrome.

Jeffrey C Horowitz, Zongbin Cui, Thomas A Moore, Tamara R Meier, Raju C Reddy, Galen B Toews, Theodore J Standiford, Victor J Thannickal

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Innate Immunity, Epithelial Plasticity, and Remodeling in Asthma.Advances in experimental medicine and biology · 2023
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  7. Characterization of Burn Eschar Pericytes.Journal of clinical medicine · 2020
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  8. Article
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  11. Mechanisms for the Resolution of Organ Fibrosis.Physiology (Bethesda, Md.) · 2019
    Review
  12. Article
  13. The matricellular protein CCN1 enhances TGF-β1/SMAD3-dependent profibrotic signaling in fibroblasts and contributes to fibrogenic responses to lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  14. Therapeutic targeting of acute lung injury and acute respiratory distress syndrome.Translational research : the journal of laboratory and clinical medicine · 2016
    Review
  15. Article
  16. Article
  17. Outstaying their Welcome: The Persistent Myofibroblast in IPF.Austin journal of pulmonary and respiratory medicine · 2014
    Article
  18. Apoptosis and angiogenesis: an evolving mechanism for fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Review
  19. X-linked inhibitor of apoptosis regulates lung fibroblast resistance to Fas-mediated apoptosis.American journal of respiratory cell and molecular biology · 2013
    Article
  20. 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

8 authors at 1 institution in 1 country.

Jeffrey C HorowitzDiv. of Pulmonary and Critical Care Medicine, Univ. of Michigan Medical Center, 6301 MSRB III, 1150 W. Medical Center Dr., Ann Arbor, MI 48109, USA.
Zongbin Cui
Thomas A Moore
Tamara R Meier
Raju C Reddy
Galen B Toews
Theodore J Standiford
Victor J Thannickal
University of Michigan–Ann Arbor · US

Funding

SCCOR in Translational Research in Acute Lung InjuryP50HL074024 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STANDIFORD, THEODORE J. · 2003 to 2007
$13.5M
Oxidants and TGF-beta in Myofibroblast Differentiation/SurvivalR01HL067967 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THANNICKAL, VICTOR J. · 2001 to 2011
$2.7M
Mesenchymal Cell Survival Signalling by TGF-B1K08HL081059 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOROWITZ, JEFFREY C · 2005 to 2009
$661k
NHLBI NIH HHS K08 HL081059NHLBI NIH HHS K08 HL-81059NHLBI NIH HHS L30 HL081881NHLBI NIH HHS P50 HL074024NHLBI NIH HHS P50 HL-81059NHLBI NIH HHS R01 HL067967NHLBI NIH HHS R01-HL-67967
6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by stereotypic host inflammatory and repair cellular responses; however, mechanisms regulating the resolution of ARDS are poorly understood. Here, we report the isolation and characterization of a novel population of mesenchymal cells from the alveolar space of ARDS patients via fiber-optic bronchoscopy with bronchoalveolar lavage (BAL). BAL was performed on 17 patients during the course of ARDS. Immunofluorescence staining and multiparameter flow cytometric analysis defined a population of alveolar mesenchymal cells (AMCs) that are CD45-/prolyl-4-hydroxylase+/alpha-smooth muscle actin+/-. AMCs proliferated in ex vivo cell culture for multiple passages; early passage (3-5) cells were subsequently analyzed in 13 patients. AMCs isolated from patients with persistent or nonresolving ARDS (ARDS-NR, n = 4) demonstrate enhanced constitutive activation of prosurvival signaling pathways involving PKB/Akt, FKHR, and BCL-2 family proteins compared with AMCs from patients with resolving ARDS (ARDS-R, n = 9). Exogenous transforming growth factor-beta1 markedly induces PKB/Akt activation in AMCs from ARDS-R. ARDS-NR cells are more resistant to serum deprivation-induced apoptosis compared with ARDS-R. This study identifies a novel population of mesenchymal cells that can be isolated from the alveolar spaces of ARDS patients. AMCs in patients with ARDS-NR acquire an activational profile characterized by enhanced prosurvival signaling and an antiapoptotic phenotype. These findings support the concept that apoptosis of mesenchymal cells may be an essential component of normal repair and resolution of ARDS and suggest that dysregulation of this process may contribute to persistent ARDS.

Indexed as

ActinsAdultAgedApoptosisBronchoalveolar Lavage FluidBronchoscopyCell ProliferationCell SurvivalFemaleFibroblastsFlow CytometryFluorescent Antibody TechniqueForkhead Box Protein O1Forkhead Transcription FactorsHumansLeukocyte Common AntigensActinsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanLeukocyte Common AntigensProcollagen-Proline DioxygenaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID16214815
PMCPMC1382273
OpenAlexW1985026480

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.