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HDAC1 Regulation of Endothelial NO

Award Number: F31HL149235
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/01/2019
PERIOD OF PERFORMANCE END DATE: 12/22/2021

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HDAC1 Regulation of Endothelial NO - PROJECT SUMMARY Excess sodium intake accounts for billions of healthcare dollars every year. In 2010, 1.65 million deaths from cardiovascular disease were attributed to a high salt diet. Furthermore, sodium intake directly correlates with kidney function and mortality. A high salt diet causes cardiovascular and renal damage by increasing oxidative stress and impairing endothelial nitric oxide (NO) signaling. The mechanisms by which a high salt diet leads to NOS3 uncoupling and increased NADPH oxidase 2 (Nox2) expression and activity remains elusive. NOS3 uncoupling is characterized by an increase in NOS-dependent reactive oxygen species (ROS) and a decrease in NOS-dependent NO. The central hypothesis to the proposed studies is that high salt increases endothelial HDAC1 which uncouples NOS3 via post-translational modification (deacetylation) and increases Nox2 expression and activity via a transcriptional mechanism. In order to study the role of HDAC1 in NOS3 uncoupling, intra-renal arteries and renal endothelial cells will be isolated from normal and high salt fed rats. HDAC1 activity as well as HDAC1 dependence of NOS3 uncoupling and NOS3 acetylation will be assessed. We will generate vascular endothelial HDAC1 knockout (VEHDAC1KO) mice to investigate the necessity of HDAC1 in high salt disrupted NO signaling. The juxtamedullary nephron preparation will be used to assess NO signalling in small intra-renal arteries. In order to identify which NOS3 lysines are susceptible to HDAC1 deacetylation, we will utilize NOS3 constructs containing specific lysine (K) to arginine (R) or glutamine (Q) mutations. Cdh5- CreERT2-Nox2KO mice will be used to assess the role of endothelial Nox2 in high salt disrupted NO signaling in small intra-renal arteries. We will use VEHDAC1KO mice to elucidate the role of HDAC1 in high salt increased Nox2 complex expression. ChIP-qPCR will be utilized to assess the effect of HDAC1 on histone modifications at the promoters of the genes of the Nox2 complex. The long-term goal of this project is to understand the role of HDAC1 in endothelial NO signaling in order to develop novel therapies for cardiovascular disease.


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: 2023 ( Subtotal = $0 )
2023	2021	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	002	3	1/19/2023	NON-COMPETING CONTINUATION	$0
2023	2020	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	001	2	1/19/2023	NON-COMPETING CONTINUATION	$0
2023	2019	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	1	1/19/2023	NEW	$0
														Subtotal = $0

Issue Date FY: 2022 ( Subtotal = -$25,318 )
2022	2021	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	3	2/10/2022	NON-COMPETING CONTINUATION	-$25,318
														Subtotal = -$25,318

Issue Date FY: 2021 ( Subtotal = $39,302 )
2021	2021	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	3	8/18/2021	NON-COMPETING CONTINUATION	$39,302
														Subtotal = $39,302

Issue Date FY: 2020 ( Subtotal = $38,786 )
2020	2020	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	2	8/21/2020	NON-COMPETING CONTINUATION	$38,786
														Subtotal = $38,786

Issue Date FY: 2019 ( Subtotal = $38,282 )
2019	2019	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	001	1	8/16/2019	NEW	$0
2019	2019	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Cardiovascular Diseases Research	000	1	8/16/2019	NEW	$38,282
														Subtotal = $38,282

Grand Total All Awards = $91,052

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HDAC1 Regulation of Endothelial NO

Award Number: F31HL149235

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/01/2019

PERIOD OF PERFORMANCE END DATE: 12/22/2021

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