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Genome‐wide analysis of circadian oscillations in gene expression in lung and its implications in lung homeostasis, repair and diseases
Author(s) -
Sukumaran Siddharth,
Jusko William J,
Dubois Debra C,
Almon Richard R
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1061.3
Subject(s) - circadian rhythm , biology , gene , gene expression , circadian clock , clock , endogeny , gene expression profiling , period (music) , microbiology and biotechnology , medicine , genetics , endocrinology , physics , acoustics
This study examines the circadian regulation of gene expression in rat lungs. A rich time series involving 54 animals sacrificed at 18 distinct time points within the 24‐h cycle was performed with mRNA expression in lung examined using Affymetrix gene chips. Data mining identified 652 genes showing robust circadian oscillations in expression in lung which were parsed into 8 distinct temporal clusters. Surprisingly more than two‐thirds of the genes showing circadian expression peaked during the animal's light/inactive period. Six core clock genes and 9 clock‐related genes showed rhythmic oscillations in their expression in lung. Many of the genes that peaked during the inactive period included genes related to extracellular matrix, cytoskeleton and protein processing and are mainly involved in the repair and remodeling of the organ. Genes coding for growth factors and its receptors that play important roles in maintaining normal lung function also showed circadian expression. In addition, genes involved in the metabolism of endogenous compounds, xenobiotics and therapeutic drugs also exhibited circadian oscillations along with genes that are biomarkers or therapeutic targets for many lung diseases, suggesting an important role for circadian rhythms in regulating various aspects of the physiology and pathophysiology of the organ. This work was supported by grant GM 24211 from NIGMS, NIH, Bethesda, MD.

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