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.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Resource-Related Research Projects--Cooperative Agreements (U24)
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Vanderbilt University Medical Center
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Gupta, Madhu; Solanki, Malvika H; Chatterjee, Prodyot K et al. (2014) Maternal magnesium deficiency in mice leads to maternal metabolic dysfunction and altered lipid metabolism with fetal growth restriction. Mol Med 20:332-40
Kang, Li; Mayes, Wesley H; James, Freyja D et al. (2014) Matrix metalloproteinase 9 opposes diet-induced muscle insulin resistance in mice. Diabetologia 57:603-13
Barnes, Tammy M; Otero, Yolanda F; Elliott, Amicia D et al. (2014) Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas. Am J Physiol Endocrinol Metab 307:E896-905
Babaev, Vladimir R; Hebron, Katie E; Wiese, Carrie B et al. (2014) Macrophage deficiency of Akt2 reduces atherosclerosis in Ldlr null mice. J Lipid Res 55:2296-308
Patel, Manishkumar; Gleason, Alexa; O'Malley, Stacey et al. (2014) Non-invasive bioluminescence imaging of ?-cell function in obese-hyperglycemic [ob/ob] mice. PLoS One 9:e106693
Cordoba-Chacon, Jose; Gahete, Manuel D; McGuinness, Owen P et al. (2014) Differential impact of selective GH deficiency and endogenous GH excess on insulin-mediated actions in muscle and liver of male mice. Am J Physiol Endocrinol Metab 307:E928-34
Lee, Stacey; Page-McCaw, Patrick; Gamse, Joshua T (2014) Kctd12 and Ulk2 partner to regulate dendritogenesis and behavior in the habenular nuclei. PLoS One 9:e110280
Zhu, Lin; Martinez, Melissa N; Emfinger, Christopher H et al. (2014) Estrogen signaling prevents diet-induced hepatic insulin resistance in male mice with obesity. Am J Physiol Endocrinol Metab 306:E1188-97
Huang, Xuan; Hernandez, Ciria C; Hu, Ningning et al. (2014) Three epilepsy-associated GABRG2 missense mutations at the ?+/?- interface disrupt GABAA receptor assembly and trafficking by similar mechanisms but to different extents. Neurobiol Dis 68:167-79
Freeman, Megan Culler; Graham, Rachel L; Lu, Xiaotao et al. (2014) Coronavirus replicase-reporter fusions provide quantitative analysis of replication and replication complex formation. J Virol 88:5319-27

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