Related Experiment Video
Updated: Dec 29, 2025

07:47
Isolation of Lung Retinoid-Containing Cells by Cell Sorting
Published on: April 11, 2025
604
Maternal vitamin D deficiency induces transcriptomic changes in newborn rat lungs
Erica Mandell1, Sharon Ryan1, Gregory J Seedorf1
1Pediatric Heart Lung Center, Department of Pediatrics, University of Colorado, Denver Anschutz Medical Center, Aurora, CO, USA.
The Journal of Steroid Biochemistry and Molecular Biology
|February 3, 2020
Summary
Maternal Vitamin D deficiency (VDD) during pregnancy alters fetal lung development, impacting airway, alveolar, and vascular growth. This study reveals VDD disrupts innate immune pathways and anabolic signaling, contributing to abnormal lung development.
Area of Science:
- Developmental Biology
- Immunology
- Genomics
Background:
- Vitamin D deficiency (VDD) in pregnancy is prevalent and linked to adverse maternal and fetal outcomes.
- Vitamin D (VD) is crucial for normal lung development, and VDD can lead to abnormal airway, alveolar, and vascular growth in neonates.
Purpose of the Study:
- To identify molecular pathways affected in the lungs of offspring exposed to maternal VDD using an unbiased transcriptomic approach.
Main Methods:
- RNA was extracted from the lungs of newborn offspring from VD-replete and VDD dams.
- Affymetrix microarrays were used for transcriptomic analysis.
- Differential gene expression and pathway enrichment analyses were performed.
Main Results:
- 2233 differentially expressed transcripts were identified between VDD and control offspring lungs.
- Suppressed pathways included vascular biology, insulin-like growth factor-1 receptor (IGF-1R), fibroblast growth factor (FGF), and cell cycle control.
- Upregulated pathways were predominantly related to the innate immune system, including granulocyte/macrophage development and cytokine signaling (Jak/Stat).
Conclusions:
- Maternal VDD during fetal development induces significant alterations in lung gene expression beyond angiogenic pathways.
- These transcriptomic changes are associated with abnormal lung growth and may create a proinflammatory environment contributing to impaired lung development.

