With the advent of genetic engineering, mice have become the preferred model for assigning physiologic function to specific genes and, in many instances, for elucidating mechanisms of human diseases. The small size and rapid heart rate of mice provide specific challenges to their use in studies of cardiovascular physiology. The need for specialized equipment and training often limits investigations of mouse cardiovascular pathophysiology. Core B houses state-of-the-art technology with the temporal and spacial resolution necessary for reliable, high throughput physiologic phenotyping of mice. All of the Core's staff, including its director, its trained microvascular surgeon, and its cardiovascular physiologist have extensive experience using mice as preclinical models. The function of the core will be to provide a centralized facility for performing all mouse vascular phenotyping and disease models for the PPG investigators. Core B will (1) perform blood pressure measurements; (2) obtain aortic compliance determinations; (3) acquire and interpret indices of cardiac output; (4) perform and interpret echocardiography for assessment of left ventricular structure and function; (5) assist with bone marrow transplantation experiments; (6) conduct all mouse surgeries, in particular, the endoluminal arterial injury model used by all three investigators; (7) monitor all animals post-operatively; (8) enter experimental results into a common database available to all projects; (9) perform all perfusion and organ isolations for experiments involving immunohistochemical analysis. The Core will provide to the investigators technology and expertise that their individual laboratories do not have. It is anticipated that the use of a common core will facilitate interactions among the PPG investigators and, by conducting the studies in a standardized manner, will allow the investigators to directly compare data.
| Lozhkin, Andrey; Vendrov, Aleksandr E; Pan, Hua et al. (2017) NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis. J Mol Cell Cardiol 102:10-21 |
| Sun, Qi-An; Runge, Marschall S; Madamanchi, Nageswara R (2016) Oxidative stress, NADPH oxidases, and arteries. Hamostaseologie 36:77-88 |
| Vendrov, Aleksandr E; Vendrov, Kimberly C; Smith, Alberto et al. (2015) NOX4 NADPH Oxidase-Dependent Mitochondrial Oxidative Stress in Aging-Associated Cardiovascular Disease. Antioxid Redox Signal 23:1389-409 |
| Madamanchi, Nageswara R; Runge, Marschall S (2013) Redox signaling in cardiovascular health and disease. Free Radic Biol Med 61:473-501 |
| Zhou, Rui-Hai; Vendrov, Aleksandr E; Tchivilev, Igor et al. (2012) Mitochondrial oxidative stress in aortic stiffening with age: the role of smooth muscle cell function. Arterioscler Thromb Vasc Biol 32:745-55 |
| Ren, Hong Yu; Patterson, Cam; Cyr, Douglas M et al. (2011) Reconstitution of CHIP E3 ubiquitin ligase activity. Methods Mol Biol 787:93-103 |
| Aitsebaomo, Julius; Srivastava, Siddharth; Zhang, Hua et al. (2011) Recombinant human interleukin-11 treatment enhances collateral vessel growth after femoral artery ligation. Arterioscler Thromb Vasc Biol 31:306-12 |
| Ronnebaum, Sarah M; Patterson, Cam (2010) The FoxO family in cardiac function and dysfunction. Annu Rev Physiol 72:81-94 |
| Madamanchi, Nageswara R; Runge, Marschall S (2010) NADPH oxidases and atherosclerosis: unraveling the details. Am J Physiol Heart Circ Physiol 298:H1-2 |
| Runge, Marschall S; Molnar, Kimberly; Madamanchi, Nageswara R (2010) ""Old"" hearts and arteries: the role of oxidative stress. Trans Am Clin Climatol Assoc 121:52-8; discussion 59-60 |
Showing the most recent 10 out of 25 publications
