Abstract

The purpose of the Cardiovascular Pathophysiology and Complications Core (CPCC) is to provide comprehensive and reproducible screening for cardiovascular disease and complications of diabetes in genetic mouse models. Many of the mouse phenotyping tests used by this Core are largely modeled after and directly translatable to tests used to assess patients with diabetes. Other procedures are reliant on novel surgical techniques for providing stimuli to the cardiovascular system or for kidney transplantation. Core services include assessment of a) cardiac morphology and function;b) vascular regulation;c) exercise capacity and metabolic function;d) circulating markers;e) models of myocardial injury and repair;and f) vascular atherosclerosis. The range of phenotyping tests performed by the CPCC allows for thorough investigation ofthe presence, correlation with and modification or amelioration of diabetic complications associated with specific genetic manipulations in the mouse.

Public Health Relevance

Cardiovascular disease, including atherosclerosis and lipid abnormalities comprise the major morbidity and mortality in diabetes. The Cardiovascular Pathophysiology and Complications Core has a range of unique phenotyping tests for genetic mouse models that are designed to better understand the devastating complications of diabetes.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Resource-Related Research Projects--Cooperative Agreements (U24)
Project #
5U24DK059637-14
Application #
8708035
Study Section
Special Emphasis Panel (ZDK1-GRB-S)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
14
Fiscal Year
2014
Total Cost
$197,524
Indirect Cost
$70,906

  Institution

Name
Vanderbilt University Medical Center
Department
Type
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212

  Publications

Hughey, Curtis C; Trefts, Elijah; Bracy, Deanna P et al. (2018) Glycine N-methyltransferase deletion in mice diverts carbon flux from gluconeogenesis to pathways that utilize excess methionine cycle intermediates. J Biol Chem 293:11944-11954
Williams, Ian M; Valenzuela, Francisco A; Kahl, Steven D et al. (2018) Insulin exits skeletal muscle capillaries by fluid-phase transport. J Clin Invest 128:699-714
Yao, Lina; Seaton, Sarah Craven; Ndousse-Fetter, Sula et al. (2018) A selective gut bacterial bile salt hydrolase alters host metabolism. Elife 7:
Kook, Seunghyi; Qi, Aidong; Wang, Ping et al. (2018) Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes. Am J Respir Cell Mol Biol 58:566-574
Pollins, Alonda C; Boyer, Richard B; Nussenbaum, Marlieke et al. (2018) Comparing Processed Nerve Allografts and Assessing Their Capacity to Retain and Release Nerve Growth Factor. Ann Plast Surg 81:198-202
Babaev, Vladimir R; Huang, Jiansheng; Ding, Lei et al. (2018) Loss of Rictor in Monocyte/Macrophages Suppresses Their Proliferation and Viability Reducing Atherosclerosis in LDLR Null Mice. Front Immunol 9:215
Fensterheim, Benjamin A; Young, Jamey D; Luan, Liming et al. (2018) The TLR4 Agonist Monophosphoryl Lipid A Drives Broad Resistance to Infection via Dynamic Reprogramming of Macrophage Metabolism. J Immunol 200:3777-3789
Harris, Nicholas A; Isaac, Austin T; Günther, Anne et al. (2018) Dorsal BNST ?2A-Adrenergic Receptors Produce HCN-Dependent Excitatory Actions That Initiate Anxiogenic Behaviors. J Neurosci 38:8922-8942
Mani, Bharath K; Castorena, Carlos M; Osborne-Lawrence, Sherri et al. (2018) Ghrelin mediates exercise endurance and the feeding response post-exercise. Mol Metab 9:114-130
Ehrlicher, Sarah E; Stierwalt, Harrison D; Newsom, Sean A et al. (2018) Skeletal muscle autophagy remains responsive to hyperinsulinemia and hyperglycemia at higher plasma insulin concentrations in insulin-resistant mice. Physiol Rep 6:e13810

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