Abstract

The application of genetic engineering to the murine cardiovascular system has yielded considerable information regarding the signaling pathways and regulation of the heart. Previously, there had been limited information regarding the relevance of these alterations to cardiovascular physiology. The advent of miniaturized electronics and improved microsurgical techniques has enabled the assessment of the physiologic effects of these genetic manipulations and has extended the understanding of the importance of these alterations. The purpose of the Hemodynamic Laboratory Core is to provide the Investigators of each Project the means by which the physiologic and pathophysiologic importance of their specific genetic interventions can be investigated. Methods to be used include studies of the ex vivo heart, in vivo cardiac catheterization, in vivo echocardiography, and application of these techniques to a rodent model of myocardial infarction and heart failure.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
1P01HL068738-01A1
Application #
6652379
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
2002-08-01
Project End
2007-07-31
Budget Start
2002-08-01
Budget End
2003-07-31
Support Year
1
Fiscal Year
2002
Total Cost
$308,662
Indirect Cost

  Institution

Name
Northern California Institute Research & Education
Department
Type
DUNS #
City
San Francisco
State
CA
Country
United States
Zip Code
94121

  Publications

Karliner, Joel S (2013) Sphingosine kinase and sphingosine 1-phosphate in the heart: a decade of progress. Biochim Biophys Acta 1831:203-12
Kawabori, Masahito; Kacimi, Rachid; Karliner, Joel S et al. (2013) Sphingolipids in cardiovascular and cerebrovascular systems: Pathological implications and potential therapeutic targets. World J Cardiol 5:75-86
Lovett, David H; Mahimkar, Rajeev; Raffai, Robert L et al. (2013) N-terminal truncated intracellular matrix metalloproteinase-2 induces cardiomyocyte hypertrophy, inflammation and systolic heart failure. PLoS One 8:e68154
Lovett, David H; Mahimkar, Rajeev; Raffai, Robert L et al. (2012) A novel intracellular isoform of matrix metalloproteinase-2 induced by oxidative stress activates innate immunity. PLoS One 7:e34177
Dahi, Sia; Karliner, Joel S; Sarkar, Rajabrata et al. (2011) Transgenic expression of matrix metalloproteinase-2 induces coronary artery ectasia. Int J Exp Pathol 92:50-6
Vessey, Donald A; Li, Luyi; Jin, Zhu-Qiu et al. (2011) A sphingosine kinase form 2 knockout sensitizes mouse myocardium to ischemia/reoxygenation injury and diminishes responsiveness to ischemic preconditioning. Oxid Med Cell Longev 2011:961059
Kotlyar, Alexander B; Randazzo, Antonio; Honbo, Norman et al. (2010) Cardioprotective activity of a novel and potent competitive inhibitor of lactate dehydrogenase. FEBS Lett 584:159-65
Wang, Guan-Ying; Yeh, Che-Chung; Jensen, Brian C et al. (2010) Heart failure switches the RV alpha1-adrenergic inotropic response from negative to positive. Am J Physiol Heart Circ Physiol 298:H913-20
Chatterjee, Kanu; Zhang, Jianqing; Honbo, Norman et al. (2010) Doxorubicin cardiomyopathy. Cardiology 115:155-62
Tao, Rong; Hoover, Holly E; Honbo, Norman et al. (2010) High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate. Am J Physiol Heart Circ Physiol 298:H1022-8

Showing the most recent 10 out of 56 publications