SEX AND STRESS HORMONES CONTROL ADRENAL GLAND MACROPHAGE DEVELOPMENT AND FUNCTION" - PROJECT SUMMARY/ABSTRA…
Federal financial assistance recorded from USAspending. This is not a procurement contract.
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ASST_NON_R01AI165553_075 · REGENTS OF THE UNIVERSITY OF MINNESOTA · Department of Health and Human Services
Compare Multiple AI Models with SmartSoloExplore CaptureIQ IntelligenceAssistance award details
- Assistance award identifier
- ASST_NON_R01AI165553_075
- FAIN
- R01AI165553
- Recipient
- REGENTS OF THE UNIVERSITY OF MINNESOTA
- Awarding agency
- Department of Health and Human Services
- Funding agency
- Department of Health and Human Services
- Assistance listing (CFDA)
- 93.855
- Total obligated
- $2,225,085
- Period
- Jun 1, 2022 – May 31, 2027
- Fiscal year
- 2022
- Place of performance state
- MN
- Source file
- FY2022_All_Assistance_Full_20261006.zip
Description
SEX AND STRESS HORMONES CONTROL ADRENAL GLAND MACROPHAGE DEVELOPMENT AND FUNCTION" - PROJECT SUMMARY/ABSTRACT: CHRONIC STRESS PROMOTES A SYSTEMIC INFLAMMATORY RESPONSE THAT CONTRIBUTES TO CARDIOVASCULAR AND METABOLIC DISEASE (CVD), AND EVEN ACUTELY AUGMENTED STRESS CAN EXACERBATE DISEASE SEVERITY. IN HUMANS, CONSUMPTION OF HIGH FAT/HIGH CHOLESTEROL DIET (HFD) IS A COMMON CO-FACTOR DRIVING CHRONIC STRESS RESPONSES. UNDERSTANDING MECHANISMS CONTROLLING THE STRESS-RESPONSE AND ITS ASSOCIATION WITH CVD DISEASES, WHICH ARE NEARLY UBIQUITOUS AND A LEADING CAUSE OF MORTALITY, WILL ALLOW FOR DEVELOPMENT OF IMPACTFUL TRANSLATIONAL APPROACHES TO FIGHT AGAINST THIS UNDERSTUDIED DISEASE. THE AG IS THE PRIMARY SOURCE FOR STEROID HORMONES, CORTICOSTERONE AND ALDOSTERONE THAT ARE PRODUCED IN THE CORTEX. ELEVATED CORTICOSTERONE MODIFIES GLUCOSE HOMEOSTASIS, IMMUNITY, AND TISSUE REMODELING. OUR PRIOR WORK USING A COLD-TEMPERATURE STRESS MODEL SHOWED THAT COLD-STRESS DRIVES THE PROMOTION OF MONOCYTE EGRESS FROM BONE MARROW AND EXACERBATED ATHEROSCLEROSIS. THEREFORE, WE SOUGHT TO DETERMINE WHETHER THE LOCAL IMMUNE CELLS IN THE AG WERE ALSO RESPONDING TO STRESS RESPONSES, EITHER THROUGH COLD-EXPOSURE OR HFD FEEDING. INTERESTINGLY, WE OBSERVED ACCUMULATION OF LIPID WITHIN AG RESIDENT MACROPHAGES SITTING ADJACENT TO HORMONE-PRODUCING ENDOCRINE CELLS IN MODELS OF ATHEROSCLEROSIS, HYPERTENSION, OR ACUTE COLD CHALLENGE. TISSUE RESIDENT MACROPHAGES ARE TYPICALLY TISSUE REPAIR CELLS AND LIPID ACCUMULATION IS ASSOCIATED WITH ANTI-INFLAMMATORY PHENOTYPES IN MACROPHAGES. AG MACROPHAGES HAVE NOT BEEN THOROUGHLY DESCRIBED IN LITERATURE, AND THEIR FUNCTION IN RESPONSE TO HORMONE SIGNALS IS UNKNOWN. THROUGH OUR PRELIMINARY STUDIES OF WT MICE (CHOW-DIET FED WITH NO OVERT STRESSORS), WE IDENTIFIED TWO PRIMARY POPULATIONS OF MACROPHAGES PRESENT IN THE AG. THESE POPULATIONS SHOWED A SEXUAL DIMORPHISM IN THE REPRESENTATION OF MACROPHAGE SUBSETS WHEN COMPARING ADULT MALE VERSUS FEMALE MICE. FURTHERMORE,