The Impact of Estrogen Deficiency and Caveolin Scaffolding Domain Peptide in the Pathogenesis of Myocardial Fibrosis Following Acute Sympathetic Stimulation

Authors' Affiliations

Cristiana Faith-Marie Martinez, Department of Biological Sciences, Crimsyn Price, Department of Biological Sciences, Lydia Lewis, Department of Biological Sciences, Pearl McCuistion, Department of Biological Sciences, Danisha Davis, Department of Biological Sciences, Krishna Singh, Department of Biomedical Sciences, East Tennessee State University.

Location

D.P. Culp Center Ballroom

Start Date

4-5-2024 9:00 AM

End Date

4-5-2024 11:30 AM

Poster Number

83

Name of Project's Faculty Sponsor

Cerrone Foster

Faculty Sponsor's Department

Biological Sciences

Classification of First Author

Undergraduate Student

Competition Type

Competitive

Type

Poster Presentation

Presentation Category

Health

Abstract or Artist's Statement

Cardiovascular disease is the leading cause of death among males and females in the United States. Sex differences are evident in the pathophysiology of cardiovascular disease. A key mechanism of heart failure is cardiac remodeling resulting in structural changes in the integrity of the heart. One example is cardiac fibrosis, which results from excessive deposits of extra cellular matrix and collagen proteins leading to stiffness of the heart and impaired mechanical function. Studies show these parameters are increased in post-menopausal aging women. We therefore examined the effects of estrogen loss and its role in pathogenesis of myocardial fibrosis in mice experiencing acute sympathetic stimulation. To examine this, mice were ovariectomized at 2.5 months and SHAM (mock) surgery was performed at 2.5 months. To examine the duration of estrogen depletion on fibrosis, mice were treated with ISO at 5 months post OVX for 3 days (ISO+OVX). We also wanted to examine if a membrane rich protein caveolin-1 scaffolding domain (CSD) would alleviate adverse remodeling from estrogen loss therefore mice were also treated with CSD for 3 days (ISO+OVX+CSD). Animals were euthanized, and the hearts were excised and sectioned at 4µm thick to analyze cardiac fibrosis using Masson’s Trichrome staining. Results are still in progress. We expect ovariectomy will result in increased myocardial fibrosis compared to SHAM. Initial results show that CSD was not protective in ovariectomized mice. We expect treatment with isoproterenol will further increase fibrosis in the ISO+OVX group and CSD would further increase fibrosis (ISO+OVX+CSD). The findings of this study can aid in understanding of heart disease in post-menopausal women.

This document is currently not available here.

Share

COinS
 
Apr 5th, 9:00 AM Apr 5th, 11:30 AM

The Impact of Estrogen Deficiency and Caveolin Scaffolding Domain Peptide in the Pathogenesis of Myocardial Fibrosis Following Acute Sympathetic Stimulation

D.P. Culp Center Ballroom

Cardiovascular disease is the leading cause of death among males and females in the United States. Sex differences are evident in the pathophysiology of cardiovascular disease. A key mechanism of heart failure is cardiac remodeling resulting in structural changes in the integrity of the heart. One example is cardiac fibrosis, which results from excessive deposits of extra cellular matrix and collagen proteins leading to stiffness of the heart and impaired mechanical function. Studies show these parameters are increased in post-menopausal aging women. We therefore examined the effects of estrogen loss and its role in pathogenesis of myocardial fibrosis in mice experiencing acute sympathetic stimulation. To examine this, mice were ovariectomized at 2.5 months and SHAM (mock) surgery was performed at 2.5 months. To examine the duration of estrogen depletion on fibrosis, mice were treated with ISO at 5 months post OVX for 3 days (ISO+OVX). We also wanted to examine if a membrane rich protein caveolin-1 scaffolding domain (CSD) would alleviate adverse remodeling from estrogen loss therefore mice were also treated with CSD for 3 days (ISO+OVX+CSD). Animals were euthanized, and the hearts were excised and sectioned at 4µm thick to analyze cardiac fibrosis using Masson’s Trichrome staining. Results are still in progress. We expect ovariectomy will result in increased myocardial fibrosis compared to SHAM. Initial results show that CSD was not protective in ovariectomized mice. We expect treatment with isoproterenol will further increase fibrosis in the ISO+OVX group and CSD would further increase fibrosis (ISO+OVX+CSD). The findings of this study can aid in understanding of heart disease in post-menopausal women.