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Paul Janssen , Ph.D.
Associate Professor
The Ohio State University
Department of Physiology & Cell Biology
Department of Internal Medicine,
Division of Cardiovascular Medicine
200 Hamilton Hall
1645 Neil Avenue
Columbus, OH 43210
Phone: (614) 247-7838
Email:
janssen.10@osu.edu
Education & Training:
Utrecht University, Netherlands, 1994 B.S.& M.S.
in Medical Biology
Utrecht University, Netherlands, 1997 Ph.D. in Cardiac
Physiology
Universities of Freiburg and Göttingen, Germany, 2000 Postdoctoral
Fellow
Johns Hopkins University, Baltimore, 2002 Research Associate
Research Interest:
Research in the Janssen lab focuses on various aspects of myocardial
relaxation. Cardiac relaxation is no longer thought to be a mere
passive process that logically follows contraction, but is a highly regulated
process, involving interactions between calcium removal systems and mechanical
molecular motors. We study relaxation using a minimalized systems
approach, in which we have the advantage of working in a sub-organ level
model (multicellular trabeculae) that still encompasses all the electrical,
biochemical, and contractile functions of the whole heart, yet is small
enough to control in vitro while allowing for assessment of intracellular
events, such as calcium transients. More than half of the patients
suffering from heart failure (which kills more people than all cancers
and aids combined) suffer from relaxation disorders, and part of our work
is to gain understanding in the molecular events that change during progression
to heart failure. Using multicellular preparations, under near-physiological
conditions, we assess contractile parameters and intracellular calcium
handling. In addition to the investigation of physiological relaxation,
impaired relaxation is studies in several models, including pulmonary artery
banded rabbits, and in various transgenic models in collaborative effects. Additional
research areas of interest in the lab, often in collaboration with other
labs are aimed at understanding the role of hydroxyl-radical induced damage
to the heart, inotropic therapy using glycolysis intermediates, the role
of junction proteins in the heart, and cardiac insufficiency in muscular
dystrophy disease.
Selected Publications:
- Varian KD, Janssen PML. Frequency dependent acceleration of relaxation
involves decreased myofilament calcium sensitivity. Am. J. Physiol.
Heart. Circ. Physiol. 2007;292:H2212-2219.
- Hiranandani N, Raman S, Kalyanasundaram A, Periasamy M, Janssen PML.
Frequency-dependent contractile strength in mice over- and under-expressing
the sarcoplasmic reticulum calcium ATPase. Am. J. of Physiol. Reg.
Integr. Comp. Physiol. 2007;293:R30-R36.
- Bupha-Intr T, Holmes JW, Janssen PML. Induction of hypertrophy in
vitro by mechanical loading in adult rabbit myocardium. Am J. Physiol.
Heart Circ. Physiol. 2007;293:H3759-H3767.
- Monasky MM, Varian KD, Janssen PML. Gender comparison of contractile
performance and b-adrenergic response in isolated rat cardiac trabeculae.
J. Comp. Physiol. Biochem. 2008;178:307-313.
- Monasky MM, Varian KD, Davis JP, Janssen PML. Dissociation of Force
Decline from Calcium Decline by Preload in Isolated Rabbit Myocardium.
Eur J Physiol., 2008;178:267-276.
- Torres CAA, Varian KD, Janssen PML. Variability in interbeat duration
influences myocardial contractility in rat cardiac trabeculae. Open
Cardiovascular Medicine Journal, 2008; 2: 100-104.
- Janssen PML, Zeitz O, Schumann H, Holtz J, Hasenfuss G. Load-induced
apoptosis in cultured multicellular preparations is unaltered in presence
of the b-adrenoceptor antagonist nebivolol. Pharmacology, 2009;83:141-147.
- Monasky MM, and Janssen PML. The positive force-frequency relationship
is maintained in absence of sarcoplasmic reticulum function in rabbit,
but not in rat myocardium. J. Comp. Physiol. B. 2009; 179: 469-479.
- Martin PT, Xu R, Rodino-Klapac LR, Oglesbay E, Camboni M, Montgomery
CL, Shontz K, Chicoine LG, Clark KR, Sahenk Z, Mendell JR, Janssen
PML. Overexpression of Galgt2 in skeletal muscle prevents injury resulting
from eccentric contractions in both mdx and wild type mice. Am
J Physiol Cell Physiol. 2009; 263: C476-488.
- Bupha-Intr T, Haizlip KM, Janssen PML.
Temporal changes in expression of connexin-43 after load-induced
hypertrophy in vitro. Am J Physiol Heart Circ Physiol. 2009; 296: H806-814.
- Varian KD, Kijtawornrat A, Gupta SC, Torres CA, Monasky MM, Hiranandani N, Delfin DA, Rafael-Fortney JA, Periasamy M, Hamlin RL, Janssen PM. Impairment of diastolic function by lack of frequency-dependent myofilament desensitization rabbit right ventricular hypertrophy. Circ Heart Fail. 2009, 2:472-481.
- Billman GE, Nishijima Y, Belevych AE, Terentyev D, Xu Y, Haizlip KM, Monasky MM, Hiranandani N, Harris WS, Gyorke S, Carnes CA, Janssen PM. Effects of Dietary Omega-3 Fatty Acids on Ventricular Function in Dogs with Healed Myocardial Infarctions: In Vivo and In Vitro Studies. Am J Physiol Heart Circ Physiol. 2010, 298:H1219-1228.
- Kota J, Handy CR, Haidet AM, Montgomery CL, Eagle A, Rodino-Klapac LR, Tucker D, Shilling CJ, Therlfall WR, Walker CM, Weisbrode SE, Janssen PM, Clark KR, Sahenk Z, Mendell JR, Kaspar BK. Follistatin gene delivery enhances muscle growth and strength in nonhuman primates. Sci Transl Med., 2009, 1:6ra15.
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