The purpose of the Molecular Biology and Analytical Core (Core B) is to centralize molecular analysis, cloning, laser capture microdissection, radioimmunoassays (RIA), enzyme activity assays, and analytical chemistry. Analytical chemistry, radioimmunoassay, enzyme immunosorbent assays, real time RT-PCR and cloning of siRNAs into shuttle vectors are of fundamental importance for state-of-the-art hypertension and renal research. Core B will perform a number of labor-intensive and time-consuming analyses that will relieve investigators from having to conduct these assays themselves and thereby allow them more time to pursue their scientific efforts. The molecular biology aspect of the core will aid investigators by cloning, performing laser capture microdissection, real time RT-PCR and genotyping knockout animals. The analytical aspect of the core will use RIA to measure cAMP and cGMP, and will also determine Ang I as an index of renin activity and/or concentration. Enzyme activity assays will also be performed for phosphodiesterase activity, phosphatidylinositol 3 kinase (PIS kinase) activity, and Akt activity. Analytical chemistry will be performed to determine calcium and sodium concentrations. Centralizing of analytical and molecular studies in Core B will ensure cost efficiency in terms of labor and laboratory facilities/equipment by eliminating duplication of effort by individual investigators. It will also help integrate projects by providing consistent and reliable assays which promote both quality and productivity for participating projects.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL090550-05
Application #
8448095
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
2015-03-31
Budget Start
2013-04-01
Budget End
2014-03-31
Support Year
5
Fiscal Year
2013
Total Cost
$230,508
Indirect Cost
$73,164
Name
Henry Ford Health System
Department
Type
DUNS #
073134603
City
Detroit
State
MI
Country
United States
Zip Code
48202
Gordish, Kevin L; Beierwaltes, William H (2014) Resveratrol induces acute endothelium-dependent renal vasodilation mediated through nitric oxide and reactive oxygen species scavenging. Am J Physiol Renal Physiol 306:F542-50
Ortiz-Capisano, M Cecilia; Reddy, Mahendranath; Mendez, Mariela et al. (2013) Juxtaglomerular cell CaSR stimulation decreases renin release via activation of the PLC/IP(3) pathway and the ryanodine receptor. Am J Physiol Renal Physiol 304:F248-56
Atchison, Douglas K; Beierwaltes, William H (2013) The influence of extracellular and intracellular calcium on the secretion of renin. Pflugers Arch 465:59-69
Ortiz-Capisano, M Cecilia; Atchison, Douglas K; Harding, Pamela et al. (2013) Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway. Am J Physiol Renal Physiol 305:F1209-19
Ramseyer, Vanesa D; Garvin, Jeffrey L (2013) Tumor necrosis factor-ýý: regulation of renal function and blood pressure. Am J Physiol Renal Physiol 304:F1231-42
Beierwaltes, William H (2013) Endothelial dysfunction in the outer medullary vasa recta as a key to contrast media-induced nephropathy. Am J Physiol Renal Physiol 304:F31-2
Atchison, Douglas K; Harding, Pamela; Beierwaltes, William H (2013) Vitamin D increases plasma renin activity independently of plasma Ca2+ via hypovolemia and *-adrenergic activity. Am J Physiol Renal Physiol 305:F1109-17
Cabral, Pablo D; Garvin, Jeffrey L (2013) Less potassium coming out, less sodium going in: phenotyping ROMK knockout rats. Hypertension 62:240-1
Ren, Yilin; D'Ambrosio, Martin A; Wang, Hong et al. (2012) Mechanisms of carbon monoxide attenuation of tubuloglomerular feedback. Hypertension 59:1139-44
Beierwaltes, William H (2012) Are microRNAs the key to transforming renin progenitor cells in the afferent renal circulation? Am J Physiol Renal Physiol 302:F27-8

Showing the most recent 10 out of 27 publications