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dc.contributor.authorSoumyaroop Bhattacharyaen_US
dc.contributor.authorDiana Goen_US
dc.contributor.authorDaria L. Krenitskyen_US
dc.contributor.authorHeidi L. Huycken_US
dc.contributor.authorSiva Kumar Solletien_US
dc.contributor.authorValerie A. Lungeren_US
dc.contributor.authorLeon Metlayen_US
dc.contributor.authorSorachai Srisumaen_US
dc.contributor.authorSusan E. Werten_US
dc.contributor.authorThomas J. Marianien_US
dc.contributor.authorGloria S. Pryhuberen_US
dc.contributor.otherUniversity of Rochester Medical Centeren_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherCincinnati Children's Hospital Medical Centeren_US
dc.date.accessioned2018-06-11T05:06:37Z-
dc.date.available2018-06-11T05:06:37Z-
dc.date.issued2012-08-15en_US
dc.identifier.citationAmerican Journal of Respiratory and Critical Care Medicine. Vol.186, No.4 (2012), 349-358en_US
dc.identifier.issn15354970en_US
dc.identifier.issn1073449Xen_US
dc.identifier.other2-s2.0-84865281335en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865281335&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/14688-
dc.description.abstractRationale: Bronchopulmonary dysplasia (BPD) is a major complication of premature birth. Risk factors for BPD are complex and include prenatal infection and O 2 toxicity. BPD pathology is equally complex and characterized by inflammation and dysmorphic airspaces and vasculature. Due to the limited availability of clinical samples, an understanding of the molecular pathogenesis of this disease and its causal mechanisms and associated biomarkers is limited. Objectives: Apply genome-wide expression profiling to define pathways affected in BPD lungs. Methods: Lung tissue was obtained at autopsy from 11 BPD cases and 17 age-matched control subjects without BPD. RNA isolated from these tissue samples was interrogated using microarrays. Standard gene selection and pathway analysis methods were applied to the data set. Abnormal expression patterns were validated by quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry. Measurements and Main Results: We identified 159 genes differentially expressed in BPD tissues. Pathway analysis indicated previously appreciated (e.g., DNA damage regulation of cell cycle) as well as novel (e.g., B-cell development) biological functions were affected. Three of the five most highly induced genes were mast cell (MC)-specific markers. We confirmed an increased accumulation of connective tissue MC TC (chymase expressing) mast cells in BPD tissues. Increased expression of MC TC markers was also demonstrated in an animal model of BPD-like pathology. Conclusions: We present a unique genome-wide expression data set from human BPD lung tissue. Our data provide information on gene expression patterns associated with BPD and facilitated the discovery that MC TC accumulation is a prominent feature of this disease. These observations have significant clinical and mechanistic implications. Copyright © 2012 by the American Thoracic Society.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865281335&origin=inwarden_US
dc.subjectMedicineen_US
dc.titleGenome-wide transcriptional profiling reveals connective tissue mast cell accumulation in bronchopulmonary dysplasiaen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1164/rccm.201203-0406OCen_US
Appears in Collections:Scopus 2011-2015

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