# Role of Vitamin D in Lung Development and Bronchopulmonary Dysplasia

> **NIH NIH K08** · UNIVERSITY OF COLORADO DENVER · 2024 · $161,899

## Abstract

The Clinical Problem: Bronchopulmonary dysplasia (BPD), the chronic lung disease of preterm infants is
associated with significant respiratory complications that continue into adulthood. BPD results from a disruption
in pulmonary vascular and alveolar growth. Recent studies suggest vitamin D plays a role in fetal lung
development and enhances lung development in an animal model of chorioamnionitis. However, the
mechanisms through which vitamin D enhances vascular and alveolar growth remain unknown.
The Candidate: I am an Assistant Professor in the Department of Pediatrics, and board certified Neonatologist
at the University Colorado School of Medicine. My studies on the effects of vitamin D on lung growth and
function were the first to demonstrate a striking protective effect of early vitamin D treatment in an animal
model of BPD, and further show that at least part of these effects are mediated through enhanced or preserved
pro-angiogenic signaling mechanisms after lung injury. My short-term goals: 1) advance my understanding
and use of mouse genetics to study mechanistic regulation of vitamin D and lung development; 2) develop new
skills to analyze and interpret genomic and genetic data to determine vitamin D-sensitive pathways during fetal
lung development; 3) expand my understanding and skills in statistics and bioinformatics. My long-term
career goal is to become an independent physician scientist who will effectively translate mechanistic
basic studies in pulmonary vascular development into new insights regarding the pathogenesis and
potential treatment of BPD. During the fourth year of this award period, I will submit my first R01 application.
The Research: Based on current literature and our preliminary data, the central hypothesis to this proposal is
that abnormal vitamin D signaling in experimental BPD contributes to abnormal vascular and alveolar
growth, causes PH, and increases susceptibility to the adverse effects of perinatal injury on lung
structure and that the pro-angiogenic effects of vitamin D in the developing lung are mediated through
increased PPARγ and VEGF signaling. We propose the following specific aims: Aim #1: To determine
whether fetal vitamin D deficiency impairs endothelial cell growth, function, and angiocrine signaling pathways,
which causes abnormal vascular and airspace structure, and increases susceptibility to postnatal hyperoxia;
Aim #2: To determine whether perinatal vitamin D signaling enhances lung structure by preserving PPARγ –
VEGF signaling in the fetal rat lung after endotoxin exposure and prevents BPD and PH; Aim #3: To determine
whether impaired vitamin D signaling due to EC-specific vitamin D receptor deficiency disrupts lung growth,
causes PH and increases the severity of lung injury to antenatal (ETX) or postnatal (hyperoxia) stress.
The Environment: I have strong multidisciplinary mentorship by established investigators (University of
Colorado School of Medicine and Purdue University). My mentor...

## Key facts

- **NIH application ID:** 10765733
- **Project number:** 5K08HL150222-05
- **Recipient organization:** UNIVERSITY OF COLORADO DENVER
- **Principal Investigator:** Erica Wynne Mandell
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $161,899
- **Award type:** 5
- **Project period:** 2020-02-15 → 2026-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10765733

## Citation

> US National Institutes of Health, RePORTER application 10765733, Role of Vitamin D in Lung Development and Bronchopulmonary Dysplasia (5K08HL150222-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10765733. Licensed CC0.

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