BIOGRAPHICAL SKETCH
NAME
Pinz, Ilka / POSITION TITLE
Scientist I
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.)
INSTITUTION AND LOCATION / DEGREE
(if applicable) / YEAR(s) / FIELD OF STUDY
Technical Univ. of Darmstadt, Darmstadt, Germany / M.S. / 1990-1996 / Zoology & Biochemistry
Alfred-Wegener Inst. for Polar and Marine Research, Bremerhaven, Germany / Ph.D. / 1996-2000 / Physiology
Research Fellow, Dept. Medicine, Brigham & Women’s Hospital, Harvard Medical School, Boston, MA / Postdoctoral / 2000-2003 / Cardiology
Senior Research Associate, Dept. Pharmacology
University of New England, Biddeford, ME / Postdoctoral / 2003-2004 / Molecular Cardiology

A. Positions and Honors

Positions and Employment

1996-2000 Research Assistant, Alfred-Wegener Institute for Polar and Marine Research, Bremerhaven, Germany

2000-2003 Research Fellow, Dept. of Medicine, Brigham & Women’s Hospital, Harvard Medical School, Boston, MA

2003-2004 Senior Research Associate in the Department of Pharmacology, Univ. of New England, Biddeford, ME

2005-present Scientist, Maine Medical Center Research Institute, Center of Molecular Medicine, Scarborough, ME

2005-present Adjunct Assistant Professor, Institute for Molecular Biophysics University of Maine, Orono, ME

2007-present Adjunct Assistant Professor, Graduate School of Biomedical Sciences, University of Maine, Portland, ME

2008-present Adjunct Assistant Professor, University of New England, Biddeford, ME

Honors

2003 American Heart Association, Travel award to attend the AHA meeting in Orlando, FL

2004 Mount Desert Island Biological Laboratory, New Investigator Award, Characterization of the role of AMP-activated protein kinase in temperature adaptation of marine invertebrates, Co-PI

Study section

2006 - 2007 American Heart Association, Northeast Consortium NEA 1B, Member

2008 – present American Heart Association, Founders Affiliation, R1 Cardiac Biology 1, Member

Other Experience and Professional Membership

2003 - Present American Physiology Society - Member

2004 - Present American Heart Association - Member

2005 - Present International Society for Magentic Resonance in Medicine - Member

2008 The European Journal of Pharmacology - Reviewer

B. Peer-Reviewed Publications

Pinz I. & H.O. Pörtner: Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen dept? J. Appl. Physiol. 2003, 94: 1177-1183,

Javadpour M., Tardiff J. C., Pinz I., Ingwall J. S.: Decreased energetics in murine hearts bearing the R92Q mutation in cradiac troponin T. J. Clin. Invest. 2003, 112: 768-775

Nascimben L., Ingwall J. S., Lorell B. H., Pinz I., Schultz V., Tornheim K., Tian R.: Mechanisms for increased glycolysis in the hypertrophied rat heart. Hypertension 2004, 44(5): 662-667

Pinz I., Robbins J., Rajasekaran N.S., Benjamin I.J., Ingwall J.S.: Unmasking different mechanical and energetic roles for the small heat shock proteins CryAB and HSPB2 in transgenic mouse hearts. FASEB J. 2008 Jan; 22(1): 84-92.

Pinz I, Ostroy SE, Hoyer K, Osinska H, Robbins J, Molkentin JD, Ingwall JS.: Calcineurin-induced energy wasting in a transgenic mouse model of heart failure. Am J Physiol Heart Circ Physiol. 2008 Mar; 294(3): H1459-66.

Pinz I, Wax SD, Anderson P, Ingwall JS: Low over-expression of TNFa in the mouse heart increases contractile performance via TNFR1. Journal of Cellular Biochemistry, 2008, 105(1): 99-107.

Urs U, Roudabush A, O’Neill C, Pinz I, Prudovsky I, Kacer D, Liaw L, Small D: Soluble forms of the Notch ligands Delta1 and Jagged1 promote in vivo tumorigenicity in NIH3T3 fibroblasts with distinct phenotypes. American Journal of Pathology, 173(3):865-78.

In preparation

Miao W, Pinz I, Williams B, Schoen F, Meister M, Tian R, Neer E, Mende U, Ingwall JS: cardiac expression of activated Gaq52 leads to decreased contractile performance in response to inotropic stimulation in isolated 17 day old mouse hearts.

Pinz I, Zhou M, Mende U, Ingwall JS: Improved Isolation Procedure for Adult Mouse Cardiomyocytes Preserves Myocyte Energetic State.

Cebova M, Knowles C, Preda M, Pinz I: Low TNFa Expression Protects the Mouse Heart from Palmitate Induced Systolic Dysfunction.

Cebova M, Knowles C, Preda M, Pinz I: Palmitate exposure of mice in utero causes systolic and vascular dysfunction via modified lipid raft structure in the offspring.

Abstracts

Pinz I, Wax S, Javadpour M, Mann D, Ingwall JS: TIA-1-/- mouse hearts exhibit improved contractile performance, similar to TNFa overexpressers. Meeting of the American Heart Association, Anaheim, CA, November 10-14 2001

Bock C, Pinz I, Poertner H-O: Metabolic changes induced by hypoxia in the brain of the amphibian Bufo marinus, observed wirh flow weighted and T2* weighted MR imaging. Proc. Intl. Soc. Mag. Reson. Med 9, 2001:677

Pinz I, Wawrousek E, Benjamin I, Ingwall JS: Deficiency of aB-crystallin and HSPB2 impairs contractile function and decreases energetics after myocardial ischemia. 46th annual meeting of the Biophysical Society, San Francisco, CA, February 23-27 2002

Pinz I, Wax SD, Anderson PD, Ingwall JS: Low overexpression of TNFa in TIA-1-/- hearts is associated with improved recovery after global ischemia. Meeting of the American Heart Association, Chicago, IL, November 17-20 2002

Pinz I: Comparison of the American and German university systems. Why study abroad? Seminar for second year undergraduate biology students at Purdue University, West Lafayette, IN, November 22 2002

Pinz I, Ostroy SE, Molkentin J, Ingwall JS: Defect of energy - mechanical transduction in mouse hearts overexpressing calcineurin. Experimental Biology, San Diego, CA, April 10-15 2003

Pinz I, Christians E, Wawrousek E, Robbins R, Benjamin I, Ingwall JS: aB-crystallin and HSPB2, two small heat shock proteins, have distinct physiological functions in the mouse heart. Meeting of the American Heart Association, Orlando, FL, November 9-13 2003

Wenfeng M, Pinz I, Williams B, Mende U, Ingwall SJ: Increased Galphaq mediated signaling in the mouse heart leads to blunted contractile performance upon inotropic stimulation and lactate-dehydrogenase switch prior to hypertrophy. Meeting of the American Heart Association, Orlando, FL, November 9-13 2003

Pinz I, Mende U, Zhu M, Balschi JA, Liao R, Ingwall JS:Isolating ventricular mouse cardiomyocytes in the presence of creatine and purine nucleosides improves energetic state. Experimental Biology, Washington, D.C., April 17-21 2004

Dube N, Mason MM, Pinz I, Davidoff AJ: PKCbII inhibition improves mechanical dysfunction in diabetic cardiomyocytes. Experimental Biology, Washington, D.C., April 17-21 2004

Dube N, Slocum K, Pinz I, Davidoff, AJ: Diabetic Cardiomyocyte Dysfunction is Reversed by PKC b Isoform Specific Inhibition. Maine Biological and Medical Sciences Symposium at Mount Desert Island Biological Laboratory, Salisbury Cove, ME April 29-30 2004

Pinz I, Christians E, Wawrousek E, Robbins R, Benjamin I, Ingwall JS: aB-crystallin and HSPB2, two small heat shock proteins, have distinct physiological functions in the mouse heart. Maine Biological and Medical Sciences Symposium at Mount Desert Island Biological Laboratory, Salisbury Cove, ME April 29-30 2004

Pinz I, Carmody MW, Dube N, Slocum K, Davidoff AJ: Hexosamine biosynthesis pathway is involved in glucose and fatty acid induced cardiomyocyte dysfunction. 2nd annual Symposium of the American Heart Association Council on Basic Cardiovascular Sciences - Targeting Heart Failure: New Science, New Tools, New Strategies, Keystone, CO July 24-27 2005

Cebova M, Knowles C, Pinz I: High Palmitate Feeding Induces Systolic Dysfunction in the Isolated Mouse Heart. 1st Biennial National IDeA Symposium of Biomedical Research Excellence (NISBRE), Washington, DC July 20-22 2006

Cebova M, Knowles C, Jackson S, Pinz I: Low TNFa Expression Protects the Mouse Heart from Palmitate Induced Systolic Dysfunction. Experimental Biology, Washington, D.C., April 28- May 2 2007

Cebova M, Knowles C, Preda M, Vary C, Pinz I: Low TNFa Expression Protects the Mouse Heart from Palmitate Induced Systolic Dysfunction. 2nd annual meeting Northeast COBRE and INBRE programs, Burlington, VT August 15 – 17, 2007

Cebova M, Knowles C, Preda M, Vary C, Pinz I: Maternal obesity "rafting" offspring toward cardiovascular disease: Palmitate exposure in utero causes systolic and vascular dysfunction via modified lipid raft structure. Circulation, in press, AHA Scientific Session, Orlando, FL November 4-7, 2007

Cebova M, Knowles C, Vary C, Pinz I: Low levels of TNFa prevent ceramide accumulation in cardiac cell membranes and lipid-induced systolic dysfunction. American Heart Association Basic Cardiovascular Sciences Conference 2008 - Heart Failure: Molecular Mechanisms and Therapeutic Targets, July 28-31, 2008, Keystone, CO

C. Research Support

ONGOING

NIH COBRE, P20 RR01555 – Project 6 PI 07/01/05 - 06/30/10

Mechanisms of Dyslipidemia in Cardiac Muscle – Goals: To define cardiac energetics in high cholesterol and high fat fed mice and the development of cardiac in vivo MRI techniques in mice.

NIH, 1 RO1 AR054604-01, PI Clifford Rosen, MD 03/15/07 – 03/14/11

Title: Mouse models to delineate a unique metabolic and skeletal network.

Role in project: Subcontract PI, performing MRI experiments to assess marrow adiposity and total body fat : body water ratios.

PENDING

American Heart Association, Scientist Development Grant, PI Ilka Pinz, PhD 01/01/09 - 12/31/11

Title: Cardiac ceramide levels determine caveolar structure and eNOS localization and activity.

Goals: To define lipid-induced changes in eNOS activation and intracellular localization.

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Ilka Pinz, Ph.D.