# Biomaterial Models of Ancestral Contributions to Wound Healing

> **NIH NIH R35** · UNIVERSITY OF FLORIDA · 2022 · $362,560

## Abstract

PROJECT ABSTRACT
People of African ancestry are 7X more likely to develop overgrowth of scar tissue, or keloids, compared people
of European ancestry. Fibrosis, chronic inflammation, and excessive scar formation is dictated by an individual’s
ancestral background. Ancestry, quantified in our work through three components of self-identification, genetic
ancestry, and sociocultural experiences, informs wound healing. While it is known that ancestry influences
clinical wound healing, we do not understand how ancestry influences cell function or cell to cell communication
in the wound response. Understanding ancestral contributions to cellular function is critical to interrogate wound
healing differences. We hypothesize that ancestry informs differences in cellular response in wound
healing. The overall goal of our research program is to leverage biomaterial models to interrogate ancestral
contributions in wound healing. In this work, we will interrogate monocyte innate immune cells and CD34+
progenitor stem cells. Our proposed research program will answer three key questions: 1) How does ancestry
influence cellular physiology? Preliminary work in our group demonstrates gene expression differences in
isolated peripheral blood mononuclear cells comparing self-identified African vs. European descendants. To
identify ancestral components beyond self-identification, we will interrogate genetic ancestry and sociocultural
factors to quantify ancestry. To determine how each ancestral component influences cell function, we will
conduct RNA sequencing and proteomic methodologies in tandem with mechanistic inhibitors to assess cell
function differences in monocytes and progenitor stem cells. 2) How does ancestry influence cellular
phenotype? While African ancestry is correlated with elevated scar formation, previous clinical studies do not
provide mechanistic insights into cellular phenotype that occurs within wound sites. To address this limitation,
we will leverage biomaterials and soluble factors to mimic wound extracellular matrix environments. To determine
how ancestral components influences the cell phenotype, monocyte and progenitor stem cell responses following
culture into the biomaterial microenvironments will be quantified. 3) How does ancestry correlate with the
cellular response in wound healing? Wound responses necessitate cell to cell communication. We will utilize
biomaterial models of cell-cell interaction and simulate wounding through oxidative stress injury. We will assess
how ancestry influences cell to cell communication in these wound environments via genetic and secretome
expression. This ESI-MIRA will enable my group to measure the influence of ancestry on wound healing through
manipulation of biomaterial platforms. Ultimately, the vision for my lab’s research is to discern the impact
of ancestry on wound healing differences and leverage biomaterial models to investigate health
disparities in healing.

## Key facts

- **NIH application ID:** 10499053
- **Project number:** 1R35GM147048-01
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **Principal Investigator:** Erika Michelle Moore
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $362,560
- **Award type:** 1
- **Project period:** 2022-08-15 → 2027-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10499053

## Citation

> US National Institutes of Health, RePORTER application 10499053, Biomaterial Models of Ancestral Contributions to Wound Healing (1R35GM147048-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10499053. Licensed CC0.

---

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