# Formyl peptide receptor activation induces vascular plasticity and remodeling inhypertension

> **NIH NIH R01** · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · 2022 · $372,500

## Abstract

PROJECT SUMMARY WENCESLAU, CAMILLA F.
 One of the major pathophysiological characteristics of hypertension is the presence of vascular
remodeling. Accordingly, it has been shown that 100% hypertensive subjects present small artery remodeling.
However, there is a gap in the literature in understanding the exact trigger that leads to vascular remodeling, and
this may limit our ability to adequately treat and prevent hypertension.
 Recent evidence implicates immune mechanisms in the pathophysiology of hypertension. Formyl peptide
receptor (FPR)-1 is a pattern recognition receptor which plays a crucial role in the function of the innate immune
system. In fact, one of the most powerful signaling pathways that induces actin polymerization and neutrophil
movement is mediated by FPR-1. Recently, we observed that this receptor is expressed in arteries. Therefore,
we questioned why a receptor that is crucial for immune defense and cell motility in leukocytes, would be
expressed and functional in arteries? We observed that activation of FPR-1 in arteries is important for the
temporal reorganization of actin, which rapidly induces actin polymerization.
 FPR-1 is a G-protein-coupled receptor that can bind N-formyl peptides produced by bacterial
degradation. Interestingly, mitochondria carry hallmarks of their bacterial ancestry. Consequently, both
mitochondrial and bacterial-derived peptides have a formyl group at their N-terminus. Therefore, N-formyl
peptides (NFPs), regardless of origin, are recognized by FPR-1 as pathogens and thus play a role in the initiation
of inflammation. Here, we observed for the first time that NFPs are present in the circulation of hypertensive
animals and humans. Therefore, it is plausible to suggest that synergistic action of leaky gut-derived bacteria
NFPs and cell damage-derived mitochondria NFPs lead to FPR-1 activation. Consequently, FPR-1 activation
maybe the trigger to induce vascular remodeling, via actin polymerization, and subsequently, hypertension.
 This planned research is uniquely suited to the NHLBI Early Stage Investigator (ESI)-Research Project
Grant (R01). It is innovative and has a strong, translational and multi-disciplinary research team of collaborators
that have the capabilities and expertise to make this project successful. As an independent ESI, my short-term
goal is to use state-of-art approaches, including culture-pressure myographs, genetic-engineering technologies,
and arteries from humans and animals to explore a major driving force behind vascular-immune network
dysfunction in hypertension.

## Key facts

- **NIH application ID:** 10328974
- **Project number:** 5R01HL149762-03
- **Recipient organization:** UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
- **Principal Investigator:** Camilla Ferreira Wenceslau
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $372,500
- **Award type:** 5
- **Project period:** 2021-01-15 → 2025-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10328974

## Citation

> US National Institutes of Health, RePORTER application 10328974, Formyl peptide receptor activation induces vascular plasticity and remodeling inhypertension (5R01HL149762-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10328974. Licensed CC0.

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