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Molecular Mechanisms of Stress Signaling in the Female Heart

Award Number: K01HL144882
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 01/15/2020
PERIOD OF PERFORMANCE END DATE: 12/31/2024

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Molecular Mechanisms of Stress Signaling in the Female Heart - Project Summary/Abstract The prevalence of heart attacks has increased among women between 35-50 years of age compared to men of the same age. In contrast to men, women have a higher risk of mortality and complications after a heart attack due to the under-representation of women in clinical trials, the lack of gender-tailored pharmacological treatments, and potential higher vulnerability of women than for men to traditional and emerging risk factors. Stress has emerged as an important risk factor for heart disease in women; stress levels have been shown to correlate with delayed recovery, recurrence, and increased mortality after a heart attack in women. Sex hormones are considered the critical regulators of the physiological differences between men and women in health and disease. These hormones certainly contribute to sexual dimorphism in heart disease; however, the effects of gender on the incidence and outcomes of a heart attack are more complex and are unlikely to be due to sex hormones alone. The goal of the present proposal is to define one of the signaling pathways underlying the deleterious effects of stress on female cardiac health in the setting of myocardial ischemia (heart attack). To accomplish this goal, we propose to investigate the mechanisms whereby glucocorticoids (the primary stress hormones) affects estrogen cardioprotection in myocardial ischemia by repressing serotonin activity in cardiomyocytes via glucocorticoid inhibition of estrogen transcriptional regulation of the serotonin receptor 5- HT2BR (implicated in cardioprotection through the regulation of mitochondrial function in cardiomyocytes). A decrease in serotonin activity has been associated with increased risk of myocardial infarction in depressed patients, and also polymorphisms in serotonin receptors are associated with elevated glucocorticoid response linked to cardiovascular complications, including an increased incidence of heart attacks. Therefore, we aim to elucidate estrogen regulatory mechanism of 5-HT2BR expression in the heart and the effects of glucocorticoids on estrogen-mediated 5-HT2BR signaling in ischemia/reperfusion (I/R). We hypothesize that stress exerts deleterious effects on the female heart in myocardial infarction by exacerbating mitochondrial dysfunction via glucocorticoids inhibition of estrogen transcriptional regulation of 5-HT2BR in cardiomyocytes. We will investigate this pathway by examining glucocorticoid and estrogen antagonism in cardiomyocytes, the effects of this crosstalk in I/R (in vivo studies), and the molecular and physiological effects of 5-HT2BR regulation by estrogen in mitochondrial function in ischemic conditions. If funded, this application will help me develop a scientifically independent project, acquire training in the cardiovascular field, build a research team, enhance my mentoring skills, and improve my grant writing skills to become competitive to apply to a major funding mechanism. My current institution and my mentor and co-mentor will provide me with the necessary facilities and guidance to accomplish these goals. Also, I will participate in training and career development activities that will strengthen my scientific career.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = -$80,501 )
2025	2024	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	5	5/6/2025	NON-COMPETING CONTINUATION	-$80,501
														Subtotal = -$80,501

Issue Date FY: 2024 ( Subtotal = $138,834 )
2024	2024	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	5	1/6/2024	NON-COMPETING CONTINUATION	$138,834
														Subtotal = $138,834

Issue Date FY: 2023 ( Subtotal = $138,834 )
2023	2023	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	4	1/5/2023	NON-COMPETING CONTINUATION	$138,834
2023	2023	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	001	4	8/29/2023	NON-COMPETING CONTINUATION	$0
														Subtotal = $138,834

Issue Date FY: 2022 ( Subtotal = $138,834 )
2022	2022	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	3	1/7/2022	NON-COMPETING CONTINUATION	$138,834
														Subtotal = $138,834

Issue Date FY: 2021 ( Subtotal = $138,834 )
2021	2021	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	2	1/8/2021	NON-COMPETING CONTINUATION	$138,834
														Subtotal = $138,834

Issue Date FY: 2020 ( Subtotal = $138,834 )
2020	2020	LOUISIANA STATE UNIVERSITY	1501 KINGS HWY	SHREVEPORT	LA	71103	CADDO	USA	Cardiovascular Diseases Research	000	1	1/13/2020	NEW	$138,834
														Subtotal = $138,834

Grand Total All Awards = $613,669

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Molecular Mechanisms of Stress Signaling in the Female Heart

Award Number: K01HL144882

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 01/15/2020

PERIOD OF PERFORMANCE END DATE: 12/31/2024

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