Date of Award

Spring 2026

Degree Type

Thesis

Department

Cell Biology and Anatomy

Director of Thesis

Dr. Camilla Wenceslau

Second Reader

Paul Townsend Jr.

Abstract

Hypertension affects almost one-half of adults and increases the risk of stroke, dementia, and heart failure. A key contributor to hypertension is dysfunction of endothelial cells, which line blood vessels and regulate vascular tone. Under hypertensive stress, these cells undergo endothelial-to-mesenchymal transition (EndMT), where they lose their protective endothelial identity and adopt a stiff, muscle-like phenotype. Hypertension is also characterized by inflammation, and prior work found increased expression of the immune receptor formyl peptide receptor 1 (FPR1) in hypertensive conditions. However, whether inflammatory signaling through FPR1 contributes to EndMT remains unknown. In this study, 3 experiments were conducted. First, a siRNA transfection was performed to decrease FPR1 gene expression in endothelial cells from murine mesenteric resistance arteries (MECs). Reverse transcription-quantitative chain polymerase reaction was utilized to evaluate the expression of FPR1 and endothelial and mesenchymal genes. Second, in an attempt to optimize the siRNA transfection protocol, various concentrations of lipofectamine and siRNA were added to MECs to determine which combination led to the greatest cell viability. Third, murine brain endothelial cells underwent physiological/normotensive (5%) or hypertensive (20%) mechanical stretch, with or without FPR1 or FPR2 inhibitors. Western blots assessed protein expression associated with cytoskeletal and mesenchymal features. Experimental results showed that 1) changes in FPR1 expression may be associated with early EndMT, 2) high concentrations of lipofectamine increase cell death and potentially impede transfection efficiency, and 3) FPR1 or FPR2 activity alone does not mediate the cytoskeletal remodeling expected in hypertension. By clarifying how inflammatory signaling drives harmful endothelial changes, this work explores early mechanisms underlying hypertension and potential targets to prevent disease progression.

First Page

1

Last Page

21

Rights

© 2026, Sriya Pallapothu

Available for download on Thursday, May 25, 2028

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