| Literature DB >> 27421969 |
David J Lederer1, Jason D Christie2, Joshua M Diamond2, Selim Arcasoy1, Jamiela A McDonnough1, Joshua R Sonett3, Matthew Bacchetta3, Frank D'Ovidio3, Edward Cantu4, Christian A Bermudez4, Amika McBurnie1, Melanie Rushefski2, Laurel H Kalman2, Michelle Oyster2, Carly D'Errico2, Yoshikazu Suzuki4, Jon T Giles5, Anthony Ferrante6, Matthew Lippel7, Gopal Singh3.
Abstract
Obesity is a risk factor for primary graft dysfunction (PGD), a form of lung injury resulting from ischemia-reperfusion after lung transplantation, but the impact of ischemia-reperfusion on adipose tissue is unknown. We evaluated differential gene expression in thoracic visceral adipose tissue (VAT) before and after lung reperfusion. Total RNA was isolated from thoracic VAT sampled from six subjects enrolled in the Lung Transplant Body Composition study before and after allograft reperfusion and quantified using the Human Gene 2.0 ST array. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed enrichment for genes involved in complement and coagulation cascades and Jak-STAT signaling pathways. Overall, 72 genes were upregulated and 56 genes were downregulated in the postreperfusion time compared with baseline. Long pentraxin-3, a gene and plasma protein previously associated with PGD, was the most upregulated gene (19.5-fold increase, p = 0.04). Fibronectin leucine-rich transmembrane protein-3, a gene associated with cell adhesion and receptor signaling, was the most downregulated gene (4.3-fold decrease, p = 0.04). Ischemia-reperfusion has a demonstrable impact on gene expression in visceral adipose tissue in our pilot study of nonobese, non-PGD lung transplant recipients. Future evaluation will focus on differential adipose tissue gene expression and the development of PGD after transplant. © Copyright 2016 The American Society of Transplantation and the American Society of Transplant Surgeons.Entities:
Keywords: genomics; ischemia reperfusion injury (IRI); lung (allograft) function/dysfunction; lung transplantation/pulmonology; translational research/science
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Year: 2016 PMID: 27421969 PMCID: PMC5195853 DOI: 10.1111/ajt.13964
Source DB: PubMed Journal: Am J Transplant ISSN: 1600-6135 Impact factor: 8.086