Evidence map›Paper›PMID 26386411›Full record

ArticleCellular signalling2015

VCAM-1 is a TGF-β1 inducible gene upregulated in idiopathic pulmonary fibrosis.

Marianna Agassandian, John R Tedrow, John Sembrat, Daniel J Kass, Yingze Zhang, Elena A Goncharova, Naftali Kaminski, Rama K Mallampalli, Louis J Vuga

Open access · hybridAbstract read
In one paragraph

Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Macrophage-Fibroblast Crosstalk Shapes Wound Repair Signaling In Vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Inhalable Hsa-miR-30a-3p Liposomes Attenuate Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Thrown for a loop: fibro-adipogenic progenitors in skeletal muscle fibrosis.American journal of physiology. Cell physiology · 2023
    Review
  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

9 authors at 3 institutions in 1 country.

Marianna AgassandianDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
John R TedrowDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
John SembratDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Daniel J KassDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Yingze ZhangDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Elena A GoncharovaDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, United States.
Naftali KaminskiSection of Pulmonary, Critical Care and Sleep Medicine, School of Medicine, Yale University, New Heaven, CT, United States.
Rama K MallampalliDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Medical Specialty Service Line, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA, United States. Electronic address: mallampallirk@upmc.edu.
Louis J VugaDorothy P and Richard P Simmons Center for Interstitial Lung Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States; Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States. Electronic address: vugalj@upmc.edu.
University of Pittsburgh · USVA Pittsburgh Healthcare System · USYale University · US

Funding

Regulation of Cardiolin Byosynthesis in Epithelial InjuryP01HL114453 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2014 to 2023
$21.3M
Lung Genomics Research ConsortiumRC2HL101715 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GERACI, MARK W, KAMINSKI, NAFTALI · 2009 to 2010
$11.4M
TNF-alpha Control of a Surfactant Enzyme in Lung InjuryR01HL081784 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2006 to 2024
$5.4M
F box-Induced Acute Lung Injury and ParkinR01HL096376 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2010 to 2025
$5.1M
Sepsis-Associated Immune Suppression and F-box ProteinsR01HL097376 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2009 to 2025
$5.1M
Stabilizing mitochondria in sepsisR01HL098174 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2010 to 2021
$3.6M
Molecular Phenotypes within and across disease boundaries in IPF and COPDR01HL095397 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI, SHAPIRO, STEVEN D · 2008 to 2011
$3.0M
New Molecular Targets in Pulmonary FibrosisR01HL073745 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI · 2003 to 2006
$2.8M
Gene networks beyond organ boundaries; heart, lung and pulmonary vascular diseaseU01HL108642 · NHLBI · YALE UNIVERSITY · PI AHMAD, FERHAAN, BENOS, PANAGIOTIS V · 2011 to 2014
$2.2M
Twist1 subphenotypes and pulmonary fibrosisR01HL126990 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KASS, DANIEL J · 2015 to 2019
$1.9M
Identifying Peripheral Blood Biomarkers in IPFK01HL108869 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VUGA, LOUIS JUSTINE · 2011 to 2014
$521k
SCF-based Ubiquitin E3 Ligases in the Pathobiology of PneumoniaI01BX002200 · VA · VETERANS HEALTH ADMINISTRATION · PI MALLAMPALLI, RAMA K · 2014 to 2017
–
BLRD VA I01 BX002200NHLBI NIH HHS HL073745NHLBI NIH HHS HL097376NHLBI NIH HHS HL108869NHLBI NIH HHS K01 HL108869NHLBI NIH HHS P01 HL114453NHLBI NIH HHS P01HL114453NHLBI NIH HHS P50HL0894932NHLBI NIH HHS R01 HL073745NHLBI NIH HHS R01 HL081784NHLBI NIH HHS R01 HL095397NHLBI NIH HHS R01HL095397NHLBI NIH HHS R01 HL096376NHLBI NIH HHS R01 HL097376NHLBI NIH HHS R01 HL098174NHLBI NIH HHS R01 HL126990NHLBI NIH HHS RC2 HL101715NHLBI NIH HHS RC2HL101715NHLBI NIH HHS U01 HL108642NHLBI NIH HHS U01HL108642
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic lethal interstitial lung disease of unknown etiology. We previously reported that high plasma levels of vascular cell adhesion molecule 1 (VCAM-1) predict mortality in IPF subjects. Here we investigated the cellular origin and potential role of VCAM-1 in regulating primary lung fibroblast behavior. VCAM-1 mRNA was significantly increased in lungs of subjects with IPF compared to lungs from control subjects (p=0.001), and it negatively correlated with two markers of lung function, forced vital capacity (FVC) and pulmonary diffusion capacity for carbon monoxide (DLCO). VCAM-1 protein levels were highly expressed in IPF subjects where it was detected in fibrotic foci and blood vessels of IPF lung. Treatment of human lung fibroblasts with TGF-β1 significantly increased steady-state VCAM1 mRNA and protein levels without affecting VCAM1 mRNA stability. Further, cellular depletion of VCAM-1 inhibited fibroblast cell proliferation and reduced G2/M and S phases of the cell cycle suggestive of cell cycle arrest. These effects on cell cycle progression triggered by VCAM1 depletion were associated with reductions in levels of phosphorylated extracellular regulated kinase 1/2 and cyclin D1. Thus, these observations suggest that VCAM-1 is a TGF-β1 responsive mediator that partakes in fibroblast proliferation in subjects with IPF.

Indexed as

AgedAnimalsCell ProliferationFemaleFibroblastsHumansIdiopathic Pulmonary FibrosisLungMaleMice, Inbred C57BLMiddle AgedProtein TransportTranscriptional ActivationTransforming Growth Factor beta1Up-RegulationVascular Cell Adhesion Molecule-1Transforming Growth Factor beta1Vascular Cell Adhesion Molecule-1IPFLung fibroblastsTGF-β1VCAM-1

Identifiers

PMID26386411
PMCPMC4684430
OpenAlexW1686615179

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Registered trials

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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.