ArticleAmerican journal of physiology. Cell physiology2014
Identification of a common Wnt-associated genetic signature across multiple cell types in pulmonary arterial hypertension.
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Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46citing papers in PubMed
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46 citing papers in PubMed, 68 citations in OpenAlex.
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- Non-Muscle MLCK Contributes to Endothelial Cell Hyper-Proliferation through the ERK Pathway as a Mechanism for Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Thromboxane-Prostanoid Receptor Signaling Drives Persistent Fibroblast Activation in Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2022Article
- Generation and Application of Directly Reprogrammed Endothelial Cells.Korean circulation journal · 2022Review
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- EGR1 Is Implicated in Right Ventricular Cardiac Remodeling Associated with Pulmonary Hypertension.Biology · 2022Article
- Noncanonical HIPPO/MST Signaling via BUB3 and FOXO Drives Pulmonary Vascular Cell Growth and Survival.Circulation research · 2022Article
- The updated view on induced pluripotent stem cells for cardiovascular precision medicine.Pflugers Archiv : European journal of physiology · 2021Review
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- KCNK3 Mutation Causes Altered Immune Function in Pulmonary Arterial Hypertension Patients and Mouse Models.International journal of molecular sciences · 2021Article
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- WNT Signalling in Lung Physiology and Pathology.Handbook of experimental pharmacology · 2021Article
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Authors and funding
25 authors at 5 institutions in 1 country.
James D WestDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Vanderbilt Vascular Biology Center, Nashville, Tennessee;
Eric D AustinDepartment of Pediatrics, Vanderbilt University, Nashville, Tennessee;
Christa GaskillDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
Shennea MarriottDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
Rubin BaskirDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee;
Ganna BilousovaGates Center for Regenerative Medicine and Stem Cell Biology, University of Colorado, Aurora, Colorado;
Jyh-Chang JeanBoston University, Boston, Massachusetts.
Anna R HemnesDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Vanderbilt Vascular Biology Center, Nashville, Tennessee;
Swapna MenonDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
Nathaniel C BloodworthDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee;
Joshua P FesselDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Vanderbilt Vascular Biology Center, Nashville, Tennessee;
Johnathan A KropskiDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
David IrwinGates Center for Regenerative Medicine and Stem Cell Biology, University of Colorado, Aurora, Colorado;
Lorraine B WareDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee;
Lisa WheelerDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
Charles C HongDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee; Veterans Administration Hospital, Nashville, Tennessee;
Barbara MeyrickDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee;
James E LoydDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
Aaron B BowmanDepartment of Neurology, Vanderbilt Brain Institute, Nashville, Tennessee; Vanderbilt Center for Stem Cell Biology, Nashville, Tennessee;
Kevin C EssDepartment of Pediatrics, Vanderbilt University, Nashville, Tennessee; Department of Neurology, Vanderbilt Brain Institute, Nashville, Tennessee; Vanderbilt Center for Stem Cell Biology, Nashville, Tennessee;
Dwight J KlemmGates Center for Regenerative Medicine and Stem Cell Biology, University of Colorado, Aurora, Colorado;
Pampee P YoungDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee; Vanderbilt Center for Stem Cell Biology, Nashville, Tennessee;
W David MerrymanDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee;
Darrell KottonBoston University, Boston, Massachusetts.
Susan M MajkaDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University, Nashville, Tennessee; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, Tennessee; Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, Tennessee; Vanderbilt Center for Stem Cell Biology, Nashville, Tennessee; Vanderbilt Vascular Biology Center, Nashville, Tennessee; Pulmonary Vascular Research Institute, Kochi, and AnalyzeDat Consulting Services, Kerala, India; and susan.m.majka@vanderbilt.edu.
Vanderbilt University · USUniversity of Colorado Denver · USVanderbilt Health · USUnited States Department of Veterans Affairs · USUniversity of Colorado Anschutz Medical Campus · US
Funding
University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0MVANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7MMEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3MInterventions Against the Molecular Etiology of BMPR2-induced PAHR01HL095797 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WEST, JAMES D · 2010 to 2022
$6.7MInterdisciplinary Training Program in Lung ResearchT32HL094296 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Ray Stokes Peebles · 2008 to 2026
$6.3MTransgenic and Gene Targeting CoreP30AR057212 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI KOCH, PETER J. · 2009 to 2018
$6.2MTraining Program in Stem Cell and Regenerative Developmental BiologyT32HD007502 · NICHD · VANDERBILT UNIVERSITY · PI WRIGHT, CHRISTOPHER V · 1997 to 2022
$5.4MGene-Neurotoxicant Interactions in Huntington DiseaseR01ES016931 · NIEHS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOWMAN, AARON B · 2008 to 2018
$4.5MRole of Lung MSC in EmphysemaR01HL116597 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MAJKA, SUSAN M · 2013 to 2021
$4.4MA Novel Adipocyte Population Arises From Bone Marrow Progenitor CellsR01DK078966 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI KLEMM, DWIGHT J · 2008 to 2016
$2.6MCardiac Induction by Small Molecule BMP InhibitorsR01HL104040 · NHLBI · VANDERBILT UNIVERSITY · PI HONG, CHARLES C · 2010 to 2014
$2.0MRole of p38 and p42/44 MAPK in Pulmonary Arterial HypertensionR01HL082694 · NHLBI · VANDERBILT UNIVERSITY · PI WEST, JAMES D · 2007 to 2011
$1.9MNCI NIH HHS P30 CA046934NCRR NIH HHS 1 UL1 RR-024975NCRR NIH HHS UL1 RR024975NHLBI NIH HHS F30 HL126280NHLBI NIH HHS HL-094707NHLBI NIH HHS HL-115103NHLBI NIH HHS K08 HL121174NHLBI NIH HHS K23 HL-098743NHLBI NIH HHS K23 HL098743NHLBI NIH HHS K25 HL094707NHLBI NIH HHS R01 HL-082694NHLBI NIH HHS R01 HL082694NHLBI NIH HHS R01 HL-091105NHLBI NIH HHS R01 HL091105NHLBI NIH HHS R01 HL-095797NHLBI NIH HHS R01 HL095797NHLBI NIH HHS R01 HL104040NHLBI NIH HHS R01 HL115103NHLBI NIH HHS R01 HL116597NHLBI NIH HHS R01 HL-11659701NHLBI NIH HHS T32 HL094296NIAMS NIH HHS P30 AR057212NICHD NIH HHS T32 HD007502NIDDK NIH HHS R01 DK078966NIDDK NIH HHS R21 DK094132NIDDK NIH HHS R21 DK-094132-01NIEHS NIH HHS ES-016931NIEHS NIH HHS R01 ES016931NIGMS NIH HHS 5T32 GM-007347-34NIGMS NIH HHS T32 GM007347NINDS NIH HHS 1R01 NS-078289NINDS NIH HHS R01 NS078289
Abstract
Understanding differences in gene expression that increase risk for pulmonary arterial hypertension (PAH) is essential to understanding the molecular basis for disease. Previous studies on patient samples were limited by end-stage disease effects or by use of nonadherent cells, which are not ideal to model vascular cells in vivo. These studies addressed the hypothesis that pathological processes associated with PAH may be identified via a genetic signature common across multiple cell types. Expression array experiments were initially conducted to analyze cell types at different stages of vascular differentiation (mesenchymal stromal and endothelial) derived from PAH patient-specific induced pluripotent stem (iPS) cells. Molecular pathways that were altered in the PAH cell lines were then compared with those in fibroblasts from 21 patients, including those with idiopathic and heritable PAH. Wnt was identified as a target pathway and was validated in vitro using primary patient mesenchymal and endothelial cells. Taken together, our data suggest that the molecular lesions that cause PAH are present in all cell types evaluated, regardless of origin, and that stimulation of the Wnt signaling pathway was a common molecular defect in both heritable and idiopathic PAH.
Indexed as
Cell DifferentiationCell LineCells, CulturedEndothelial CellsFamilial Primary Pulmonary HypertensionHumansHypertension, PulmonaryPluripotent Stem CellsRespiratory MucosaWnt Signaling Pathwayendothelial cellgene arrayheritable pulmonary arterial hypertensionidiopathic pulmonary arterial hypertensioninduced pluripotent stem cellmesenchymal stromal cellpulmonary arterial hypertensionWnt signaling
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