Personnel
Ilka Pinz
Principal Investigator
Maine Medical Center Research Institute
(207) 885-8280 Office
(207) 885-8179 Fax
pinzi@mmc.org
http://www.mmcri.org/cmm/pinz.html
Research:
The research focus of my laboratory is two sided. Our biochemical/physiological focus is on mechanisms leading to the development of cardiomyopathy in dyslipidemia. With the growing incidence of obesity, and the burden this puts on the health care system, it is important to understand the mechanisms how certain fatty acids and their metabolites contribute to signaling pathways in cardiomyocytes that cause a decline in contractile performance. In particular, the interaction of fatty acid metabolism and tumor necrosis factor alpha (TNF-alpha), a cytokine released by adipocytes and cardiomyocytes, are poorly understood. We utilize transgenic mouse models of dyslipidemia and TNF-alpha over-expression to investigate contractile performance in-vivo and of the isolated heart.
The magnetic resonance focus is on in vivo cardiac imaging in dyslipidemic mouse models and models of cardiac infarcts. To improve determination of the infarct area we will use magnetic nano particles that localize to the infarct area. In addition, we support a variety of projects from scientists within Maine Medical Center Research Institute, IMB and the greater New England area.
Recent Publications:
Pinz I, Pörtner HO. 2003. Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen dept? J Appl Physiol 94:1177-1183
Javadpour M, Tardiff JC, Pinz I, Ingwall JS. 2003. Decreased energetics in murine hearts bearing the R92Q mutation in cradiac troponin. J Clin Invest 112:768-775
Nascimben L, Ingwall JS, Lorell BH, Pinz I, Schultz V, Tornheim K, Tian R. 2004. Mechanisms for increased glycolysis in the hypertrophied rat heart. Hypertension 44:662-667
Pinz I, Ostroy S, Robbins J, Molkentin J, Ingwall JS. 2005. Energy demand and supply mismatch in hearts of mice over-expressing calcineurin, (submitted)
Pinz I, Robbins J, Benjamin IJ, Ingwall JS. 2005. Unmasking different mechanical and energetic roles for the small heat shock proteins CRYAB and HSPB2 using genetically modified mouse hearts, (submitted)
Pinz I, Wax SD, Javadpour M, Mann D, Anderson P, Ingwall JS. 2005. Low overexpression of TNFa in mouse hearts increases calcium sensitivity and protects the heart from ischemic damage, (in prep)
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