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Early Life Stress Mediates Vascular Dysfunction through Reprogramming of Endothelium

Award Number: F31HL184814
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/01/2026
PERIOD OF PERFORMANCE END DATE: 07/31/2028

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Early Life Stress Mediates Vascular Dysfunction through Reprogramming of Endothelium - Early life stress (ELS) is highly prevalent, encompassing abuse, neglect, assault, witnessing violence, or an unstable home environment. At least one of these events is experienced by 65% of the population during childhood and adolescence. Alarmingly, ELS increases the risk of severe health outcomes, with greater exposure correlating to higher risk. Risks of ischemic heart disease, hypertension, kidney disease, diabetes and markers of future cardiovascular complications like arterial stiffness are all elevated at earlier ages. Despite extensive epidemiological data linking ELS to cardiovascular disease (CVD), the mechanistic understanding of how these early life stressors lead to lifelong cardiovascular complications is lacking. The primary objective of this fellowship is to address this gap and identify mechanisms underlying vascular dysfunction following early life stress. Our previous work has utilized the mouse model of neglect, maternal separation with early weaning (MSEW). We found that MSEW mice exhibit endothelial dysfunction and vascular stiffness due to increased reactive oxygen species, namely superoxide production. We designed two aims to address the primary objective of the predoctoral fellowship. Aim 1 is focused on histone deacetylases (HDACs) that are implicated in cardiovascular diseases and vascular superoxide production, with our preliminary data suggesting that specifically HDAC9 is elevated in the endothelium of MSEW mice compared to controls. Thus, aim 1 will test the hypothesis that HDAC9 mediates ELS-induced endothelial dysfunction and vascular stiffness through up- regulation of NOX and increased superoxide. We will identify HDAC expression and localization as well as assess vascular function in endothelial-specific HDAC9 knockout and control mice exposed to MSEW. Aim 2 is focused on how the perception of ELS in the brain translates to whole-body vascular dysfunction. A key pathway by which stress is communicated outside the central nervous system is the adrenergic system via catecholamines. Catecholamines are implicated in vascular dysfunction following chronic stress and superoxide production in the endothelium. However, very little is known about the adrenergic system with ELS-induced vascular dysfunction. Therefore, Aim 2 will test the hypothesis that endothelial-specific β2 adrenergic receptor signaling mediates endothelial dysfunction and vascular stiffness in ELS. Experiments will analyze adrenergic receptor localization and catecholamine levels in endothelial-specific β2 adrenergic receptor knockout and control mice as well as those with β-adrenergic receptor blockade or vehicle in mice exposed to MSEW. This predoctoral F31 fellowship will be conducted in a dynamic, interactive research environment equipped with cutting edge technologies and innovative approaches as well as with access to experts in developing novel models. Additional benefits of this fellowship include the extensive professional development opportunities, active participation in translational multi-project grants, cascading mentor opportunities, and collaborating with physicians under the guidance of my advisor—experiences that will be invaluable to my long-term career growth.


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: 2026 ( Subtotal = $42,036 )
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	001	1	7/6/2026	NEW	$0
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	1	7/6/2026	NEW	$42,036
														Subtotal = $42,036

Grand Total All Awards = $42,036

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Early Life Stress Mediates Vascular Dysfunction through Reprogramming of Endothelium

Award Number: F31HL184814

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/01/2026

PERIOD OF PERFORMANCE END DATE: 07/31/2028

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