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Uteroplacental Insufficiency Alters the Retinoid Pathway and Lung Development in Newborn Rats
Liang-Ti Huang1, Hsiu-Chu Chou2, Chun-Mao Lin3
1Department of Pediatrics, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Department of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Insights
Intrauterine growth retardation (IUGR) in rats leads to abnormal lung development and altered retinoic acid (RA) signaling. This study found increased RAR-β expression, suggesting the retinoid pathway
Area of Science:
- Developmental biology
- Pulmonary medicine
- Endocrinology
Background:
- Intrauterine growth retardation (IUGR) is linked to impaired infant and adult lung function.
- The retinoic acid (RA) signaling pathway is crucial for lung development.
- Uteroplacental insufficiency may disrupt lung retinoid signaling.
Purpose of the Study:
- To investigate the hypothesis that uteroplacental insufficiency alters retinoid pathway elements in developing lungs.
- To examine the impact of IUGR on RA receptor and binding protein expression.
- To assess the effects of IUGR on lung alveolarization.
Main Methods:
- Uteroplacental insufficiency induced via bilateral uterine vessel ligation in rats (IUGR group) or sham surgery (control group) on Gestation Day 18.
- Lung tissue analysis using Western blotting, immunohistochemistry, and morphometry on Postnatal Days 3 and 7.
- Comparison of body weight, lung weight, protein expression, and alveolar structure between IUGR and control groups.
Main Results:
- IUGR rats showed significantly lower body and lung weights.
- Increased retinoic acid receptor (RAR)-β protein expression was observed in IUGR lungs on Postnatal Day 3.
- IUGR resulted in defective alveolarization, characterized by increased alveolar airspace and decreased alveolar wall fractions.
Conclusions:
- Uteroplacental insufficiency leads to defective lung alveolarization in newborn rats.
- Transient increases in RAR-β expression are associated with IUGR-induced lung abnormalities.
- The retinoid pathway is implicated as a potential mediator of lung defects resulting from uteroplacental insufficiency.
Background:
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.
