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Department of Physiology and Cell Biology   

Muthu Periasamy, PhD, Chair

Researchers in Physiology and Cell Biology work to understand the cellular and molecular mechanisms that contribute to cancer, cardiovascular, gastrointestinal and neurological disease. Taking a systematic approach, they develop animal models to investigate human diseases, study disease progression at the molecular level and explore its effect on organ physiology. The goal is to understand disease processes and identify molecular targets for clinical intervention. Faculty teach in Ohio State’s College of Medicine and in the colleges of Dentistry, Pharmacy, Optometry and Allied Medical Professions. They also participate in the Integrated Biomedical Graduate Program and mentor students from five graduate programs at Ohio State.

Ongoing Research Programs

  • The laboratory team of George Billman, PhD, investigates the effects of dietary omega-3 fatty acids (fish oil) on susceptibility to lethal cardiac arrhythmias – studies that will evaluate the effects of dietary fish supplements on arrhythmias induced in a canine model of sudden cardiac arrest. In the laboratory of Jack Boulant, PhD, scientists conduct electrophysiological studies employing intracellular recordings of neurons in rat hypothalamic tissue slices. They are characterizing neurons according to their responses to temperature and various perfusion media to test neuronal sensitivities to pH, CO2, reproductive hormones and feverproducing agents; current experiments explore the role of sodium and potassium currents that determine sensitivities of neuronal populations.
  • The main focus of the Jonathan Davis, PhD, laboratory team is to determine the cellular and molecular basis of striated muscle contraction and relaxation – calcium-dependent processes. They seek to understand how calcium binding proteins/enzymes are appropriately “tuned” kinetically in vitro and in vivo to control cellular function. In the laboratory of Sandor Gyorke, PhD, scientists are studying muscle excitation-coupling, intracellular calcium signaling, regulatory mechanisms of calcium-induced calcium release in cardiac muscle, cellular and molecular mechanisms responsible for inherited ventricular arrhythmia, and abnormal calcium handling in heart failure.
  • Lyn Jakeman, PhD, and her laboratory team study the role of astrocytes and the extracellular matrix in axonal growth and recovery after spinal cord injury. The laboratory team of Paul Jannsen, PhD, focuses on myocardial relaxation. Using intracellular measurements of ion homeostasis coupled with assessment of contractile function, they study mechanisms governing relaxation of the heart muscle in both health and disease.
  • Sissy Jhiang, PhD, and her laboratory team investigate sodium iodide symporter-mediated radionuclide imaging and targeted therapy for thyroid cancer and breast cancer. Research in the laboratory of Beth Lee, PhD, explores two aspects of bone and kidney biology. First, scientists examine how regulation of the actin cytoskeleton in osteoclasts affects these cells’ ability to degrade bone, and thus, their contribution to skeletal health; they then study how regulation of gene expression via modulation of mRNA stability helps protect renal epithelial cells from damage and death following acute kidney injury.
  • The long-term goal of the laboratory team headed by Muthu Periasamy, PhD, is to understand the role of calcium homeostasis in cardiac function and disease. Data suggest that the expression and activity of several calcium-handling proteins are altered in human heart failure; to determine how altered expression or activity of Ca2+ transport proteins cause disease, scientists use transgenic mouse models to alter Ca2+ transport and study how altered SR Ca2+ uptake or Ca2+ storage function affect cardiac function and cause heart failure. Scientists in the laboratory of Jack Rall, PhD, strive to understand mechanisms that control cardiac and skeletal muscle contraction and relaxation, and to engineer proteins that modulate these mechanisms.
  • Robert Stephens Jr., PhD, and his laboratory team study the neurobiology of chronic pain syndromes such as fibromyalgia and related algesic disorders with a central nervous system component (e.g., irritable bowel syndrome, non-ulcer dyspepsia, non-cardiac chest pain). Neuropathic pain is a focus of the laboratory, which uses transgenic murine models to investigate the role of pro-oxidant species and glutamate transporter dysfunction in mediating algesia.
  • Research in the laboratory of Arthur Strauch, PhD, centers on vascular and cardiac remodeling in the context of heart transplantation, acute inflammatory and wound-healing responses, and chronic fibrotic disease; emphasis is placed on expression of the vascular smooth muscle alpha-actin gene that becomes misregulated during dysfunctional cardiovascular remodeling and is influenced at both the transcriptional and post-transcriptional levels by injuryassociated growth factors such as TGF beta and altered levels of molecular oxygen. The laboratory of Dale Vandre, PhD, uses proteomics to identify plasma membrane proteins in human tissue and to determine changes in the expression of these proteins associated with differentiation and disease processes. Focusing on the placenta, they have identified a set of membrane repair proteins that were previously known to function only in skeletal muscle repair; these proteins are associated with limb-girdle types of muscular dystrophy, and their role in normal and diseased placentas is a focus of this lab.
  • The laboratory team of Jackie Wood, PhD, concentrates on electrophysiological investigation of signal transduction mechanisms for slow excitatory neurotransmission in intestinal secretomotor neurons in relation to diarrhea and constipation in functional gastrointestinal disorders. They also are characterizing purinergic slow excitatory postsynaptic potential that is mediated by a novel metabotropic ATP receptor (P2Y1 receptor) in the enteric nervous system (i.e., the brain-in-the-gut). Mark Ziolo, PhD, leads a research program that centers on excitation-contraction coupling in the heart, focusing on how nitric oxide and related signaling molecules alter cardiac myocyte function.

Research Accomplishments of 2007

  • G eorge Billman, PhD, and his laboratory team found that a 10-week endurance exercise training program completely suppressed the induction of ventricular fibrillation in animals previously shown to be susceptible to sudden cardiac death.
  • The laboratory team of Sandor Gyorke, PhD, showed that RyR2-mediated SR Ca(2+) leak is a major factor in the abnormal intracellular Ca(2+) handling that critically contributes to the reduced SR Ca(2+) content and contractility of failing cardiomyocytes.
  • Lyn Jakeman, PhD, and her laboratory team demonstrated that axonal growth into a spinal cord lesion cannot be overcome using a peptide that causes axons to ignore a known repellent molecule. A more effective mechanism to overcome inhibition is to alter the function of the astrocytes surrounding the injury site.
  • Researchers in the laboratory of Paul Janssen, PhD, discovered that post-translational modifications of myofilament proteins occur when heart rate changes, and that this process becomes impaired in models where cardiac function is deteriorating.
  • Muthu Periasamy, PhD, and his laboratory team demonstrated that Sarcolipin, a novel 31 amino acid molecule, regulates SR Ca2+ transport in the atria by directly inhibiting the Ca2+ transport pump. Importantly, its levels are decreased in arrhythmic heart disease, implicating its potential role in cardiac arrhythmia.
  • The laboratory of Robert Stephens Jr., PhD, established a transgenic murine model that overexpresses glutamate transporters and has reduced visceral pain after colorectal distension; this finding has been confirmed pharmacologically. Dale Vandre, PhD, and his laboratory team developed methods for purifying the apical plasma membrane of the human placental syncytiotrophoblast and completed an analysis of the proteome of this membrane. As part of these studies, they identified members of the ferlin family of membrane repair proteins in the placenta and are determining the role of these proteins in placental biology.
  • In the laboratory of Jackie Wood, PhD, scientists discovered that the drug lubiprostone (Amitiza®) prevented morphineinduced suppression of intestinal secretion in human intestine. They also demonstrated that the inflammatory mediator, radykinin, induced cyclooxygenase-2 expression and prostaglandin E2 release in the enteric nervous system. In addition, they found that spinal sensory afferent nerves innervate mast cells and evoke the release of histamine and other mast cell mediators associated with food allergy and inflammatory states in the intestine.

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