| Literature DB >> 33050709 |
Kiflai Bein1, Koustav Ganguly1,2, Timothy M Martin1, Vincent J Concel1, Kelly A Brant1, Y P Peter Di1, Swapna Upadhyay1,2, James P Fabisiak1, Louis J Vuga3,4, Naftali Kaminski3,5,4, Emrah Kostem6, Eleazar Eskin6, Daniel R Prows7, Ann-Soo Jang8, George D Leikauf1.
Abstract
In this study, a genetically diverse panel of 43 mouse strains was exposed to ammonia, and genome-wide association mapping was performed employing a single-nucleotide polymorphism (SNP) assembly. Transcriptomic analysis was used to help resolve the genetic determinants of ammonia-induced acute lung injury. The encoded proteins were prioritized based on molecular function, nonsynonymous SNP within a functional domain or SNP within the promoter region that altered expression. This integrative functional approach revealed 14 candidate genes that included Aatf, Avil, Cep162, Hrh4, Lama3, Plcb4, and Ube2cbp, which had significant SNP associations, and Aff1, Bcar3, Cntn4, Kcnq5, Prdm10, Ptcd3, and Snx19, which had suggestive SNP associations. Of these genes, Bcar3, Cep162, Hrh4, Kcnq5, and Lama3 are particularly noteworthy and had pathophysiological roles that could be associated with acute lung injury in several ways.Entities:
Keywords: ARDS; acute lung injury; chemical threat; functional genomics; transcriptomics
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Year: 2020 PMID： 33050709 PMCID： PMC7847062 DOI： 10.1152/ajplung.00276.2020
Source DB: PubMed Journal: Am J Physiol Lung Cell Mol Physiol ISSN： 1040-0605 Impact factor: 5.464