- Core C The Molecular and Biochemistry Core Facility will provide critical services to support the scientific goals of this Program Project; namely, the analysis of RAS and RAS-related genes, proteins, and biochemistry in myocardial fluid, tissue, and cells. All analyses will be done by trained personnel linked to the samples. The implementation of a complementary and uniform approach to these services will allow findings to be compared and contrasted across tissues, species, and sexes. This is a significant asset for the proposed studies as investigators in Project 1 and 2 begin to characterize the expression of systemic and cardiac RAS in transgenic rats expressing the human forms of angiotensinogen [TGR(hAGT)L1623] and human chymase (hCHY Tg+).

Public Health Relevance

- Core C This Core will provide a centralized infrastructure for all molecular and biochemical assays for the Program Project, allowing shared access to sophisticated equipment and expensive technologies, which will accelerate the overall pace of research.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL051952-25
Application #
9672542
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Program Officer
Maric-Bilkan, Christine
Project Start
Project End
2021-03-31
Budget Start
2019-04-01
Budget End
2020-03-31
Support Year
25
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Wake Forest University Health Sciences
Department
Type
DUNS #
937727907
City
Winston-Salem
State
NC
Country
United States
Zip Code
27157
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Ola, Mohammad Shamsul; Alhomida, Abdullah S; Ferrario, Carlos M et al. (2017) Role of Tissue Renin-angiotensin System and the Chymase/angiotensin-( 1-12) Axis in the Pathogenesis of Diabetic Retinopathy. Curr Med Chem 24:3104-3114
Ferrario, Carlos M; Mullick, Adam E (2017) Renin angiotensin aldosterone inhibition in the treatment of cardiovascular disease. Pharmacol Res 125:57-71
Chappell, Mark C; Al Zayadneh, Ebaa M (2017) Angiotensin-(1-7) and the Regulation of Anti-Fibrotic Signaling Pathways. J Cell Signal 2:

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