# The Role of Emergency Granulopoiesis in Wound Healing after Myocardial Infarction

> **NIH NIH F31** · UNIVERSITY OF LOUISVILLE · 2024 · $35,822

## Abstract

Myocardial infarction (MI) wound healing is accomplished through scar formation initiated by an acute
inflammatory response. The post-MI inflammatory phase is marked by a dramatic recruitment of neutrophils to
the heart where they become activated. Studies within the clinic have demonstrated that increased quantities
of circulating neutrophils serve as a predictor of death and adverse prognoses. Studies have demonstrated
that elimination of this neutrophil response prior to MI delays scar formation and contributes to worsening heart
failure. These two narratives indicate that although increased quantities of neutrophils may contribute to
pathogenesis of heart failure, a certain number are required for appropriate scar formation. Either side of this
balance could contribute to worsened cardiac function. Due to their short lifespan, the body must maintain the
number of circulating neutrophils through steady-state granulopoiesis. However, in circumstances of immune
challenge (such as in MI), the enhanced demand for neutrophil production is met through a reactive process
known as emergency granulopoiesis. Whether or not neutrophils produced through emergency granulopoiesis
exhibit different character or function has not been investigated previously and presents a gap in current
understanding. Additionally, how any altered neutrophil function may contribute to the pathogenesis of heart
failure post-MI is unknown. We hypothesize that neutrophils produced via emergency granulopoiesis exhibit
altered functions which contribute to the pathogenesis of heart failure. This project seeks to determine if
emergency granulopoiesis produces neutrophils with aberrant secretory function and if emergency
granulopoiesis contributes to post-MI heart failure. The objectives of the proposed research are 1) to determine
if MI-induced emergency granulopoiesis gives rise to neutrophils with differential functionality and 2) to
determine if emergency granulopoiesis delays scar formation and contributes to heart failure post-MI.
Successful completion of the proposed research will contribute to the knowledge of neutrophil function in
situations of inflammatory stress such as after MI and the role of neutrophils in post-MI scar formation.
Additionally, identification of differential functions and their role in the pathogenesis of heart failure could
present avenues of study for future identification of therapeutic targets facilitating post-MI recovery.

## Key facts

- **NIH application ID:** 10903097
- **Project number:** 1F31HL174069-01
- **Recipient organization:** UNIVERSITY OF LOUISVILLE
- **Principal Investigator:** Jonah Stephan
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $35,822
- **Award type:** 1
- **Project period:** 2024-08-01 → 2026-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10903097

## Citation

> US National Institutes of Health, RePORTER application 10903097, The Role of Emergency Granulopoiesis in Wound Healing after Myocardial Infarction (1F31HL174069-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10903097. Licensed CC0.

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