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Epigenetic modulation of purinergic signaling in microglia

Award Number: R03AI152213
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 03/06/2020
PERIOD OF PERFORMANCE END DATE: 02/28/2023

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Epigenetic modulation of purinergic signaling in microglia - In the brain, the innate immune response is initiated by microglia and amplified by astrocytes, which through glial communication act to propagate the neuroinflammatory response. It is well known that adenosinergic signaling is ubiquitous to the brain yet is immerging as a key regulatory mechanism that can be utilized to disrupt neuroglial communication and reduce neuroinflammation. Both microglia and astrocytes possess adenosinergic receptors and express the enzymes that metabolize extracellular ATP and adenosine which in turn modulate adenosinergic and inflammatory signaling. Because adenosine can influence neuronal activity and modulate neuroinflammation, being able to modulate adenosine levels or the receptors involved in adenosinergic signaling has a broad therapeutic potential. However, the link between acetate-induced epigenetic changes in purinergic protein expression is not well understood. Based on these studies we propose the hypothesis that increasing acetate metabolism, via increases in histone acetylation, will modulate purinergic signaling in microglia promoting an anti-inflammatory phenotype. To test this hypothesis we will complete following two aims (1) to determine the mechanism(s) by which acetate alters purine metabolism and (2) to determine the functional effect that acetate-induced changes in purinergic signaling have on inflammatory phenotype. Our working hypothesis is that acetate-induced changes in purinergic signaling will confer an anti-inflammatory phenotype my modulating histone acetylation. By describing how energy supplementation can influence the expression of enzymes and receptors involved in purinergic signaling is important to understand the therapeutic mechanism of acetate supplementation. The innovative of this study is to determine the epigenetic link between an increase in acetyl-CoA metabolism, alterations in purinergic signaling, and its functional effect on inflammatory phenotype.


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: 2024 ( Subtotal = -$1,414 )
2024	2021	UNIVERSITY OF NORTH DAKOTA	264 CENTENNIAL DR STOP 8371	GRAND FORKS	ND	58202	GRAND FORKS	USA	Allergy and Infectious Diseases Research	000	2	1/23/2024	NON-COMPETING CONTINUATION	-$1,414
														Subtotal = -$1,414

Issue Date FY: 2021 ( Subtotal = $70,500 )
2021	2021	UNIVERSITY OF NORTH DAKOTA	264 CENTENNIAL DR	GRAND FORKS	ND	58202	GRAND FORKS	USA	Allergy and Infectious Diseases Research	000	2	2/3/2021	NON-COMPETING CONTINUATION	$70,500
														Subtotal = $70,500

Issue Date FY: 2020 ( Subtotal = $70,500 )
2020	2020	UNIVERSITY OF NORTH DAKOTA	264 CENTENNIAL DR	GRAND FORKS	ND	58202	GRAND FORKS	USA	Allergy and Infectious Diseases Research	000	1	3/5/2020	NEW	$70,500
														Subtotal = $70,500

Grand Total All Awards = $139,586

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Epigenetic modulation of purinergic signaling in microglia

Award Number: R03AI152213

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 03/06/2020

PERIOD OF PERFORMANCE END DATE: 02/28/2023

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