دورية أكاديمية

Differential gene expression in the initiation and progression of nickel-induced acute lung injury.

التفاصيل البيبلوغرافية
العنوان: Differential gene expression in the initiation and progression of nickel-induced acute lung injury.
المؤلفون: McDowell SA; Department of Environmental Health, University of Cincinnati, Cincinnati, OH 45267-0056, USA., Gammon K, Bachurski CJ, Wiest JS, Leikauf JE, Prows DR, Leikauf GD
المصدر: American journal of respiratory cell and molecular biology [Am J Respir Cell Mol Biol] 2000 Oct; Vol. 23 (4), pp. 466-74.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: American Thoracic Society Country of Publication: United States NLM ID: 8917225 Publication Model: Print Cited Medium: Print ISSN: 1044-1549 (Print) Linking ISSN: 10441549 NLM ISO Abbreviation: Am J Respir Cell Mol Biol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2000- : New York, NY : American Thoracic Society
Original Publication: [New York, NY : The Association, [c1989-
مواضيع طبية MeSH: Gene Expression Profiling*, Lung/*drug effects , Nickel/*adverse effects, Animals ; DNA, Complementary ; Lung/metabolism ; Lung/pathology ; Mice ; Mice, Inbred C57BL
مستخلص: Acute lung injury, an often fatal condition, can result from a wide range of insults leading to a complex series of biologic responses. Despite extensive research, questions remain about the interplay of the factors involved and their role in acute lung injury. We proposed that assessing the temporal and functional relationships of differentially expressed genes after pulmonary insult would reveal novel interactions in the progression of acute lung injury. Specifically, 8,734 sequence-verified murine complementary DNAs were analyzed in mice throughout the initiation and progression of acute lung injury induced by particulate nickel sulfate. This study revealed the expression patterns of genes previously associated with acute lung injury in relationship to one another and also uncovered changes in expression of a number of genes not previously associated with acute lung injury. The overall pattern of gene expression was consistent with oxidative stress, hypoxia, cell proliferation, and extracellular matrix repair, followed by a marked decrease in pulmonary surfactant proteins. Also, expressed sequence tags (ESTs), with nominal homology to known genes, displayed similar expression patterns to those of known genes, suggesting possible roles for these ESTs in the pulmonary response to injury. Thus, this analysis of the progression and response to acute lung injury revealed novel gene expression patterns.
معلومات مُعتمدة: P30-ES06096 United States ES NIEHS NIH HHS; R01-HL-58275 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (DNA, Complementary)
4FLT4T3WUN (nickel sulfate)
7OV03QG267 (Nickel)
تواريخ الأحداث: Date Created: 20001006 Date Completed: 20001103 Latest Revision: 20131121
رمز التحديث: 20240627
DOI: 10.1165/ajrcmb.23.4.4087
PMID: 11017911
قاعدة البيانات: MEDLINE
الوصف
تدمد:1044-1549
DOI:10.1165/ajrcmb.23.4.4087