Steve Karlik

Research Interests

Keywords: Multiple sclerosis, experimental allergic encephalomyelitis, apoptosis, chemokine signalling, integrin-mediated neuroinflammation, spinal cord trauma

Description of Research Activities

Our laboratory has been interested in novel ways to understand and interfere with neuroinflammation observed in multiple sclerosis (MS). 

In addition to its involvement in tumour growth, angiogenesis has been implicated in the evolution of autoimmune inflammatory disorders like rheumatoid arthritis and multiple sclerosis (MS). MS is a chronic inflammatory autoimmune and demyelinating disease of the central nervous system (CNS). Although the histopathology and imaging characteristics of the disease is well defined, its etiology and molecular mechanisms remain elusive resulting in a limited therapeutic arsenal. We proposed that sufficient vascularization is required to supply MS lesions with additional inflammatory cells and, consequently, to maintain the inflammatory state. As a consequence, inhibition of angiogenesis would represent an alternative mechanism for interfering with disease progression without generalized immunosuppression. Therefore, we have undertaken the search for anti-angiogenesis molecules which might be relevant to MS and are working on non-teratogenic derivatives of thalidomide. We are investigating the physiological and cell signaling characteristics of these compounds in cellular systems and in animal models.

Also, neuropathological studies are underway with autopsied MS CNS material to investigate the role of connexin molecules in the development of and recovery from demyelinating lesions.

Selected Publications

1. VEGF and angiogenesis in acute and chronic MOG((35-55)) peptide induced EAE.
   Roscoe WA, Welsh ME, Carter DE, Karlik SJ. J Neuroimmunol. 2009 Apr 30;209(1-2):6-15

2. Preliminary biological evaluations of new thalidomide analogues for multiple sclerosis application. Contino-Pépin C, Parat A, Périno S, Lenoir C, Vidal M, Galons H, Karlik SJ, Pucci B. Bioorg Med Chem Lett. 2009 Feb 1;19(3):878-81

3. Experimental allergic encephalomyelitis in connexin 43-heterozygous mice. Roscoe WA, Kidder GM, Karlik SJ. Cell Commun Adhes. 2007 Mar-Jun;14(2-3):57-73.

4. Connexin 43 gap junction proteins are up-regulated in remyelinating spinal cord.
   Roscoe WA, Messersmith E, Meyer-Franke A, Wipke B, Karlik SJ. J Neurosci Res. 2007 Apr;85(5):945-53