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Antenatal nicotine exposure results in programming of aberrant alveolar development and interstitial pulmonary fibrosis in adult male rats
Author(s) -
DASGUPTA CHIRANJIB,
Xiao DaLiao,
Xu Zhice,
Yang Shumei,
Zhang Lubo
Publication year - 2012
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.26.1_supplement.698.10
Subject(s) - offspring , lung , ctgf , nicotine , medicine , pulmonary fibrosis , endocrinology , fetus , fibrosis , angiotensin ii , receptor , pregnancy , biology , growth factor , genetics
Objective Identification of abnormalities in lung structure, and expression of profibrotic proteins in the adult rat offspring lung exposed to maternal smoking in fetal life. Methods Antenatal nicotine exposed adult offspring lungs were analyzed for lung volume (LV), lung/body weight ratio (L/BWR), morphology, and protein expression patterns. Results Male offspring lung showed decreased radial alveolar count, thickened alveolar septa, with heightened interstitial collagen expression, angiotensin II type 1 receptor (AT1R), TGF‐ β1, and CTGF proteins. In contrast, female offspring lungs had reduced L/BWR, increased LV, and expression of angiotensin II type 2 receptor (AT2R), resulting in the decreased AT1R to AT2R ratio. Smad3 expression was down‐regulated in male but not in female lungs. Conclusions Antenatal nicotine exposure results in fetal programming of abnormal lung development linking maternal nicotine use to increased susceptibility of interstitial pulmonary fibrosis in adult male offspring lung in a sex‐dependent manner. Supported in part by NIH grant HL83966