# The Role of Myeloid Cell-Specific Epidermal Growth Factor Receptor in Cardiac Pathophysiology

> **NIH NIH F31** · TEMPLE UNIV OF THE COMMONWEALTH · 2020 · $31,851

## Abstract

PROJECT SUMMARY
A growing body of evidence suggests significant roles for myeloid cells in cardiac physiology. For one, these
leukocytes have been reported to partake in the maintenance of functional and structural homeostasis.
Additionally, after injury, myeloid cell processes can enormously influence short- and long-term remodeling and
repair outcomes. Given these paramount roles, a lot of recent work has focused on identifying and examining
exactly how these leukocytes are regulated. Epidermal growth factor receptor (EGFR) is a receptor tyrosine
kinase that is known to critically govern many cell processes including migration, proliferation and survival.
Interestingly, recent reports suggest that EGFR regulates macrophage activation and function, however it is
currently unknown if, and how EGFR might influence myeloid cell responses to ischemic injury. As such, we
have generated myeloid cell-specific EGFR knockout mice (EGFR mylKO) to determine the impact of such
deletion on acute cardiac injury outcomes. Following baseline analysis, EGFR mylKO mice exhibited increased
cardiomyocyte size, and fetal gene expression compared to aged matched floxed EGFR (EGFRf/f) controls. To
assess differences in post-injury inflammation, we subjected EGFR mylKO and controls to myocardial
infarction (MI). Within 1 week post-MI, EGFR mylKO mice displayed worse systolic function, enhanced LV
dilation, and increased immune cell presence in the heart when compared to controls. These phenotypes lead
us to question how myeloid cell-specific EGFR invokes physiological changes in the steady state and injured
heart. We hypothesize that myeloid cell-specific EGFR is crucial in regulating post-injury inflammation and
cardiac remodeling outcomes. We will address our research questions by further examining the impact of
myeloid cell EGFR deletion on cardiac structure/function (Aim 1) and determining the role of myeloid cell
EGFR deletion on cardiac myeloid cell dynamics (Aim 2). Conclusion of this work will aid in our understanding
of the mechanisms which contribute in the transition from injury to heart failure.

## Key facts

- **NIH application ID:** 10066126
- **Project number:** 1F31HL154814-01
- **Recipient organization:** TEMPLE UNIV OF THE COMMONWEALTH
- **Principal Investigator:** Ama Dedo Okyere
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $31,851
- **Award type:** 1
- **Project period:** 2020-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10066126

## Citation

> US National Institutes of Health, RePORTER application 10066126, The Role of Myeloid Cell-Specific Epidermal Growth Factor Receptor in Cardiac Pathophysiology (1F31HL154814-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10066126. Licensed CC0.

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