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Linda Kusner

Linda Kusner

Assistant Research Professor of Pharmacology & Physiology
Assistant Research Professor of Integrative Systems Biology (Secondary)

Office Phone: 202-476-1229
Email:
Department: Pharmacology & Physiology

Education

  • B.S., Cleveland State University, 1988
  • PhD, Case Western Reserve University, 2004

Biography

I started my career as a research technician at the VA Medical Center in Cleveland. After several years of fascinating meandering through the fields of biological sciences, I decided it was time to go back to school. The location was obvious since I was already on the Case Western Reserve University campus working. I obtained a Ph.D. from Case Western Reserve University in the Department of Physiology and Biophysics. My thesis focus was on the role of GAPDH in Diabetic Retinopathy. After a postdoctoral fellowship position in Neurology studying myasthenia gravis, I took a position as an Assistant Professor at Saint Louis University in the Department of Ophthalmology in 2007. Due to my interest in skeletal muscle, I joined the Research Center for Genetic Medicine at Children’s National Medical Center. My research interests focused on the understanding of extraocular muscle physiology and response to disease.  By studying the unique environment and cell specificity found in the extraocular muscle, I hope to be able to manipulate skeletal muscle during the disease state to return it to proper function.

Additional Education

Case Western Reserve University, Post-doctorate 2004-2007
Saint Louis University, Neurology, Post-doctorate 2007
Saint Louis University, Ophthalmology, Assistant Professor 2007-2011
George Washington University, Pharmacology and Physiology, Assistant Professor 2011
Children’s National Medical Center, Research Center for Genetic Medicine, Assistant Professor 2011

Publications

  • Kaminski HJ, Kusner LL, Nash KV, Ruff RL.  The gamma-subunit of the acetylcholine receptor is not expressed in the levator palpebrae superioris. Neurology 1995 Mar;45(3 Pt 1):516-8.
     
  • Kaminski HJ, Kusner LL, Block CH. Expression of acetylcholine receptor isoforms at extraocular muscle endplates. Investigative Ophthalmology & Visual Science, 1996 Feb;37(2):345-51.
     
  • Kusner LL, Kaminski HJ. Nitric oxide synthase is concentrated at the skeletal muscle endplate.  Brain Res 1996 Aug 19;730(1-2):238-42.
     
  • Kusner LL, Mygland A, Kaminski HJ.  Ryanodine receptor gene expression thymomas. Muscle Nerve 1998 Oct;21(10):1299-303.
     
  • Kusner LL, Kim E, Kaminski HJ.  Heme oxygenase-2 expression at rat neuromuscular junctions. Neurosci Lett 1999 Oct 8;273(3):143-6.
     
  • Richmonds CR, Boonyapisit K, Kusner LL, Kaminski HJ.  Nitric oxide synthase in aging rat skeletal muscle. Mech Ageing Dev 1999 Sep 8;109(3):177-89.
     
  • Sweeney WE Jr, Kusner L, Carlin CR, Chang S, Futey L, Cotton CU, Dell KM, Avner ED.  Phenotypic analysis of conditionally immortalized cells isolated from the BPK model of ARPKD.  Am J Physiol Cell Physiol 2001 Nov;281(5):C1695-705.
     
  • Porter JD, Merriam AP, Khanna S, Andrade FH, Richmonds CR, Leahy P, Cheng G, Karathanasis P, Zhou X, Kusner LL, Adams ME, Willem M, Mayer U, Kaminski HJ. Constitutive properties, not molecular adaptations, mediate extraocular muscle sparing in dystrophic mdx mice. FASEB J. 2003 May;17(8):893-5.
     
  • Kusner L, Carlin C. Potential role for a novel AP180-related protein during endocytosis in MDCK cells.  Am J Physiol Cell Physiol. 2003 Nov;285(5):C995-1008.
     
  • Kusner LL, Sarthy VP, Mohr S. Nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase: a role in high glucose-induced apoptosis in retinal Muller cells. Invest Ophthalmol Vis Sci. 2004 May;45(5):1553-61.
     
  • Kaminski HJ, Kusner LL, Richmonds C, Medof ME, Lin F. Deficiency of decay accelerating factor and CD59 leads to crisis in experimental myasthenia. Exp Neurol. 2006 Dec;202(2):287-93.
     
  • Kusner LL, Kaminski HJ, Soltys J.  The Effect of Complement and its Regulation on Myasthenia Gravis Pathogenesis. Expert Review of Clinical Immunology. 2008 Jan; 4(1): 43-52.
     
  • Soltys J, Kusner LL, Young A, Richmonds C, Hatala D, GongB, Shanmugavel V, Kaminski HJ. Novel Complement Inhibitor (rEV576) Limits Severity of Experimentally Acquired Myasthenia Gravis. Annals of Neurology. 2009 Jan;65(1):67-75.
     
  • Kusner LL, Young A, Tjoe S, Kaminski HJ. Perimysial fibroblasts of extraocular muscle are as unique as the muscle fibers. Investigative Ophthalmology & Visual Science, 2010 Jan; 51(1):192-200.

Research

My research interests focus on the understanding of extraocular muscle development, physiology, and response to disease. The goal is to determine the unique environment and cell specificity that allow for the extraocular muscles to function. The challenge lies in integration of the activities of each cell type in a complex tissue to understand their contribution to a functional and distinctive phenotype. The advent of targeted tissue-specific gene inactivation, molecular level imaging, and cell culture techniques offer opportunities to begin the task of dissecting out the interactions of cells within an organ. Adding to the complexity is the growing appreciation that “support cells” are not uniform across the body.  My work characterizes the unique nature of extraocular muscle fibroblasts and the ability for the fibroblasts to support the developing myotubes. For skeletal muscle, innervation and neuronal stimulation is another critical contributor to phenotype. I have published articles on the localization of proteins to the neuromuscular junction including the expression of the gamma-subunit of the acetylcholine receptor in the multiple innervated endplates of the extraocular muscle. Diseases that involve skeletal muscle create a unique opportunity to dissect out the complexity of extraocular muscle due to the prevalence or absence of pathophysiology. Myasthenia Gravis is an autoimmune disease in which antibodies attack the neuromuscular junction, resulting in weakness. Involvement of the ocular muscles in this disease produce severe ocular disturbance. I investigate the mechanisms of neuromuscular destruction by complement mediated lysis. The over-arching goal is to understand the extrinsic cues and the intrinsic regulatory mechanisms of extraocular muscle and specifically the mechanism that drives the diversity of the EOM phenotype.

Publications

View publications by this faculty member from January 1, 2013 - present

Additional publications published before January 1, 2013 may be available within Himmelfarb Library's database.