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Retinoid metabolism and signaling in lung from COPD patients with different degree of emphysema
Author(s) -
Roy Somdutta Sinha,
Schäffer Michael W,
Ong David E,
Das Salil K
Publication year - 2010
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.24.1_supplement.893.6
Subject(s) - retinoid , copd , retinoic acid , lung , western blot , chronic bronchitis , medicine , signal transduction , microarray analysis techniques , biology , gene expression , pathology , endocrinology , gene , microbiology and biotechnology , biochemistry
Chronic bronchitis and emphysema are two types of chronic obstructive pulmonary disease (COPD). Numerous findings suggest that retinoic acid (RA) may protect against emphysema. Vitamin A and its active metabolite RA are important for growth and differentiation of tissues. Considerable evidence demonstrates that RA is an essential signaling molecule for normal lung development. The objective of the present study is to establish a relationship between the severity of emphysema and levels of expression of genes involved in retinoid metabolism/signaling. Microarray analysis was done on samples from each of the 3 COPD groups using Human Whole Genome OneArray TM . Data show differential gene expression in the expression of 11 genes of retinoid metabolism and signaling between 3 groups (7 up‐regulated and 4 down‐regulated). Data from western blot analysis indicate a relationship between the protein levels of several mediators [LRAT, CRBP‐I, CRABP‐II, CYP26A1, RAR (α, β, γ) and RXRα] and severity of emphysema. Immunohistochemical staining of lung sections from COPD patients was done for some of these proteins and compared with the normal lung sections. Taken together, our results strongly support the hypothesis that there is a strong relationship between an abnormality in retinoid metabolism/signaling and severity of emphysema. (Supported by NIH grant 1RO3 HL095419‐01A1)