Research Assistant Professor
Dept. Anatomy and Physiology
Kansas State University
Ph.D., Cornell University, 2005
Postdoctoral, Michigan State University, 2005-2006
Postdoctoral, Kansas State University, 2006-2011
Postdoctoral, USDA-ARS-CGAHR-SPIRU, 2011-2013
Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for the alleviation of pain and inflammation, but their use is associated with a suite of negative side-effects, particularly in the gastrointestinal (GI) tract. The mechanisms underlying GI toxicity caused by NSAIDs initially was thought to arise out of indiscriminate inhibition of prostaglandin synthesis; however, mounting evidence suggests that more diverse mechanisms are involved. Disruption of intestinal restitution, the cell migration-dependent process by which defects in the intestinal epithelia are repaired, is one side-effect caused by NSAIDs that may contribute to GI damage. Our research program focuses on understanding the molecular mechanisms underlying NSAID-induced disruption of cell migration, in addition to identifying novel mechanisms through which NSAIDs disrupt normal epithelial function. Understanding how NSAID-induced toxicity occurs will allow the development of intervention strategies to alleviate symptoms and/or guide future efforts to synthesize new categories of NSAIDs that do not promote GI damage.
von Stein, F, KS Silver, DM Soderlund. 2013. Indoxacarb, Metaflumizone, and Other Sodium Channel Inhibitor Insecticides: Mechanism and Site of Action on Mammalian Voltage-Gated Sodium Channels. Pesticide Biochemistry and Physiology 106: 101-112.
Goodman CL, D Stanley, JA Ringbauer Jr, RW Beeman, KS Silver, Y Park. 2012. A cell line derived from the red flour beetle Tribolium castaneum (Coleoptera: Tenebrionidae). In Vitro Cellular & Developmental Biology – Animal 48: 426-433.
Silver, KS, A Desourmaux, LC Freeman, and JD Lillich. 2012. Expression of pleiotrophin, an important regulator of cell migration, is inhibited in intestinal epithelial cells by treatment with non-steroidal anti-inflammatory drugs. Growth Factors 30: 258-266.
Lillich, JD, W Ray-Miller, KS Silver, E Davis, and BD Schultz. 2011. Intra-abdominal hyaluronan concentration in peritoneal fluid of horses with sudden signs of severe abdominal pain. American Journal of Veterinary Research. 72: 1666-1673.
Song, W, KS Silver*, Y Du, Z Liu, K Dong. 2011. Analysis of the action of lidocaine on insect sodium channels. Insect Biochemistry and Molecular Biology 41: 36-41.
Silver, KS, L Leloup, LC Freeman, A Wells, JD Lillich. 2010. Non-steroidal anti-inflammatory drugs inhibit calpain activity and membrane localization of calpain 2 protease. International Journal of Biochemistry and Cell Biology 42: 2030-2036.
Silver, KS, W Song, Y Nomura, V Salgado, K Dong. 2010. Mechanism of action of sodium channel blocker insecticides (SCBIs) on insect sodium channels. Pesticide Biochemistry and Physiology 97: 87-92.
Silver, KS, W Song, Y Nomura, V Salgado, K Dong. 2009. Role of the sixth segment of domain IV of the cockroach sodium channel in the action of sodium channel-blocker insecticides. Neurotoxicology 30: 613-621.
Raveendran, NN, KS Silver*, LC Freeman, D Narvaez, K Weng, S Ganta, JD Lillich. 2008. Drug Induced Alterations to Gene and Protein Expression in IEC-6 Cells Suggest a Role for Calpains in the Gastrointestinal Toxicity of Nonsteroidal Anti-inflammatory Agents. Journal of Pharmacology and Experimental Therapeutics 325: 389-399.
Freeman, LC, DF Narvaez, A McCoy, FB von Stein, S Young, KS Silver, S Ganta, D Koch, R Hunter, RF Gilmour, JD Lillich. 2007. Depolarization and Decreased Surface Expression of K+ Channels Contribute to NSAID-Inhibition of Intestinal Restitution. Biochemical Pharmacology 74: 74-85.