# Deciphering Inflammatory Regulation of Oral Epithelial Progenitor Cells During Oral Mucosal Regeneration

> **NIH NIH F30** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2023 · $53,494

## Abstract

Project Summary
The oral cavity represents a unique healing environment that is relatively unexplored. Regeneration within the
oral mucosa occurs rapidly, with wounds closing at four times the rate of the skin, and the inflammatory reaction
to wounding is relatively suppressed. Chronic wounds within the oral cavity compromise the ability of patients to
obtain nutrition and are prone to debilitating infections, thus constituting an important oral health problem.
Understanding how the oral mucosa is able to achieve such regeneration, and therefore how wound healing is
disrupted in disease environments, would be a significant achievement for the field of craniofacial research. The
specific cellular mechanisms used by the oral mucosa to facilitate its distinct regenerative phenotype remain
elusive and are addressed in this proposal.
 Studies comparing dermal and oral wounds have shown that oral wound healing displays a short
inflammatory phase followed by a rapid transition into wound closure via epithelial cell proliferation, migration
and differentiation. Chronic inflammation in the oral cavity is the cause of many pathologies, such as periodontitis,
oral mucositis and osteonecrosis of the jaw, but how inflammation leads to epithelial atrophy or lingering open
wounds in the oral mucosa is unknown. Given that the oral epithelial progenitor cell (OEPC) population mediates
re-epithelialization, this proposal will test the hypothesis that inflammation acts as an important coordinator of
wound closure and re-epithelialization via direct regulation of the OEPC population. Wound healing will be
assessed in animals under three inflammatory states: normal, low and high. The effects of attenuated and
exacerbated inflammation on regeneration will be established by scoring for time to wound closure, epithelial
layer integrity and proliferation and apoptosis within the entire tissue (Aim 1). Next, the cellular and molecular
mechanisms of inflammatory regulation on the OEPC population will be determined using single cell RNA
sequencing under the three conditions, and direct regulation of the epithelium by the immune system tested
using an in vitro co-culture system (Aim 2). Data from these aims will determine how inflammation regulates
wound closure and elucidate key mechanisms through which inflammation influences re-epithelialization, which
will yield valuable insights into the mechanisms of wound closure within the oral mucosa.
 These research goals will be conducted in conjunction with a comprehensive training plan designed to
develop the applicant’s career as a dentist-scientist. The training includes structured mentorship from two highly
qualified clinician-scientist sponsors, and scientific and technical training through individual and group meetings,
seminars, journal clubs, classes and departmental events. Research and training will take place at the University
of California, San Francisco, which offers both an outstanding research environment and an ex...

## Key facts

- **NIH application ID:** 10621716
- **Project number:** 5F30DE029987-04
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Jessica Cook
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $53,494
- **Award type:** 5
- **Project period:** 2020-06-20 → 2025-06-19

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10621716

## Citation

> US National Institutes of Health, RePORTER application 10621716, Deciphering Inflammatory Regulation of Oral Epithelial Progenitor Cells During Oral Mucosal Regeneration (5F30DE029987-04). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10621716. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*