Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats

Intrauterine growth retardation (IUGR) is associated with reduced lung function during infancy and perhaps throughout adulthood. The retinoic acid (RA) signaling pathway modulates pre- and postnatal lung development. This study was conducted to test our hypothesis that uteroplacental insufficiency a...

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Main Authors: Liang-Ti Huang, Hsiu-Chu Chou, Chun-Mao Lin, Chung-Ming Chen
Format: Article
Language:English
Published: Elsevier 2016-12-01
Series:Pediatrics and Neonatology
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Online Access:http://www.sciencedirect.com/science/article/pii/S1875957216300183
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author Liang-Ti Huang
Hsiu-Chu Chou
Chun-Mao Lin
Chung-Ming Chen
author_facet Liang-Ti Huang
Hsiu-Chu Chou
Chun-Mao Lin
Chung-Ming Chen
author_sort Liang-Ti Huang
collection DOAJ
description Intrauterine growth retardation (IUGR) is associated with reduced lung function during infancy and perhaps throughout adulthood. The retinoic acid (RA) signaling pathway modulates pre- and postnatal lung development. This study was conducted to test our hypothesis that uteroplacental insufficiency alters the elements of the retinoid pathway in developing lungs. Methods: On Gestation Day 18, either uteroplacental insufficiency was induced through bilateral uterine vessel ligation (IUGR group) or sham surgery (control group) was performed. Lung tissues from the offspring were examined through Western blotting, immunohistochemistry, and morphometry on Postnatal Day 3 and Postnatal Day 7. Results: Compared with control rats, the IUGR rats exhibited significantly lower body weights on Postnatal Day 3 and Postnatal Day 7 and significantly lower lung weights on Postnatal Day 3. Uteroplacental insufficiency significantly increased RA receptor (RAR)-β protein expression on Postnatal Day 3. The expression of RAR-α, RAR-γ, cellular RA-binding protein-1, and cellular RA-binding protein-2 between the control and IUGR rats was comparable on Postnatal Day 3 and Postnatal Day 7. Compared with the control rats, the IUGR rats exhibited a significantly higher volume fraction of alveolar airspace on Postnatal Day 3 and Postnatal Day 7 and a significantly lower volume fraction of alveolar walls on Postnatal Day 3. Conclusion: Uteroplacental insufficiency causes defective alveolarization and transient increases in RAR-β expression in the lungs of newborn rats. The retinoid pathway may be one of the probable pathways mediating lung abnormalities caused by uteroplacental insufficiency.
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spelling doaj-art-40f6055ddd5b4b51ab71f8c4be2097082025-08-20T01:51:06ZengElsevierPediatrics and Neonatology1875-95722016-12-0157650851410.1016/j.pedneo.2016.03.003Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn RatsLiang-Ti Huang0Hsiu-Chu Chou1Chun-Mao Lin2Chung-Ming Chen3Department of Pediatrics, Wan Fang Hospital, Taipei Medical University, Taipei, TaiwanDepartment of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Biochemistry, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanDepartment of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, Taipei, TaiwanIntrauterine growth retardation (IUGR) is associated with reduced lung function during infancy and perhaps throughout adulthood. The retinoic acid (RA) signaling pathway modulates pre- and postnatal lung development. This study was conducted to test our hypothesis that uteroplacental insufficiency alters the elements of the retinoid pathway in developing lungs. Methods: On Gestation Day 18, either uteroplacental insufficiency was induced through bilateral uterine vessel ligation (IUGR group) or sham surgery (control group) was performed. Lung tissues from the offspring were examined through Western blotting, immunohistochemistry, and morphometry on Postnatal Day 3 and Postnatal Day 7. Results: Compared with control rats, the IUGR rats exhibited significantly lower body weights on Postnatal Day 3 and Postnatal Day 7 and significantly lower lung weights on Postnatal Day 3. Uteroplacental insufficiency significantly increased RA receptor (RAR)-β protein expression on Postnatal Day 3. The expression of RAR-α, RAR-γ, cellular RA-binding protein-1, and cellular RA-binding protein-2 between the control and IUGR rats was comparable on Postnatal Day 3 and Postnatal Day 7. Compared with the control rats, the IUGR rats exhibited a significantly higher volume fraction of alveolar airspace on Postnatal Day 3 and Postnatal Day 7 and a significantly lower volume fraction of alveolar walls on Postnatal Day 3. Conclusion: Uteroplacental insufficiency causes defective alveolarization and transient increases in RAR-β expression in the lungs of newborn rats. The retinoid pathway may be one of the probable pathways mediating lung abnormalities caused by uteroplacental insufficiency.http://www.sciencedirect.com/science/article/pii/S1875957216300183alveolarizationintrauterine growth retardationretinoic aciduteroplacental insufficiency
spellingShingle Liang-Ti Huang
Hsiu-Chu Chou
Chun-Mao Lin
Chung-Ming Chen
Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
Pediatrics and Neonatology
alveolarization
intrauterine growth retardation
retinoic acid
uteroplacental insufficiency
title Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
title_full Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
title_fullStr Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
title_full_unstemmed Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
title_short Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
title_sort uteroplacental insufficiency alters the retinoid pathway and lung development in newborn rats
topic alveolarization
intrauterine growth retardation
retinoic acid
uteroplacental insufficiency
url http://www.sciencedirect.com/science/article/pii/S1875957216300183
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