# Role of alveolar epithelial cell-derived cellular communication network factor 2 (CCN2) in alveologenesis and bronchopulmonary dysplasia

> **NIH NIH K08** · NEMOURS CHILDREN'S HOSPITAL, DELAWARE · 2023 · $162,000

## Abstract

PROJECT SUMMARY/ABSTRACT
This proposal describes a 5-year training program to provide Dr. Deepthi Alapati, MD, MS, Attending
Neonatologist at Nemours AI duPont Hospital for Children with the mentorship, training and research
experience required to become an independent clinician scientist and a leader in neonatal lung disease
research. She has received a Master’s degree in Translational Research from University of Pennsylvania.
Candidate’s long-term career goal is to develop novel therapies to promote lung repair and regeneration for
treatment of neonatal lung diseases such as bronchopulmonary dysplasia (BPD). To achieve these goals, she
will be mentored by a team of internationally recognized experts in pulmonary basic science research from
Nemours and University of Pennsylvania with whom she has a proven track record of successful mentorship
and productivity. She will undergo a rigorous didactics and hands-on training program to acquire expertise in
elucidating pulmonary cell-specific molecular mechanisms within the lung microenvironment using complex
genetic mouse models and 3D co-culture systems; application of gene editing technologies as a mechanistic
and therapeutic tool to modulate candidate genes in complex lung diseases such as BPD; and expertise in
advanced bioinformatics. Her research will focus on (1) elucidating the function of Cellular communication
network factor 2 (Ccn2) in alveolar epithelial cells (AEC) during alveologenesis and (2) evaluating whether
modulating Ccn2 expression in AEC will improve a hyperoxia-induced BPD phenotype. This research proposal
is built upon candidate’s preliminary research that demonstrates an important causative role for Ccn2 in severe
BPD and the therapeutic potential of CRISPR-Cas9 gene editing technology to manipulate disease causing
genes expressed in the developing pulmonary epithelium. BPD is the most common cause of death, severe
neurodevelopmental impairment, and hospital readmissions in preterm infants. In spite of advances in clinical
care, clinical efforts to prevent and treat BPD have been largely unsuccessful. As the cell type most exposed to
the external environment, AEC have emerged as a central focus in many lung diseases, including BPD.
Moreover, AEC can be directly targeted by therapeutic agents delivered through intra-amniotic, intra-nasal and
intra-tracheal routes. Thus, a better understanding of mechanisms in AEC that drive alveologenesis during
normal lung development and in response to early postnatal lung injury, would pave path for targeted therapies
for severe BPD. By precisely examining the spatial and temporal function of Ccn2 in AEC during
alveologenesis and early postnatal lung injury induced by hyperoxia, this study will provide novel mechanistic
insights into its role in regulating alveologenesis and lead to novel therapies targeted at AEC-derived Ccn2 for
the prevention and treatment of severe BPD. Candidate has access to all required technical, laboratory and
intell...

## Key facts

- **NIH application ID:** 10684698
- **Project number:** 5K08HL151760-04
- **Recipient organization:** NEMOURS CHILDREN'S HOSPITAL, DELAWARE
- **Principal Investigator:** Deepthi Alapati
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $162,000
- **Award type:** 5
- **Project period:** 2020-08-01 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10684698

## Citation

> US National Institutes of Health, RePORTER application 10684698, Role of alveolar epithelial cell-derived cellular communication network factor 2 (CCN2) in alveologenesis and bronchopulmonary dysplasia (5K08HL151760-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10684698. Licensed CC0.

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