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Jonathan M. King, Ph.D.

Associate Professor

 

Getting to Know Jonathan M. King...

 

My research program is interested in understanding the physiology of epithelial cell junctions. Tight junctions are important protein complexes that help hold epithelial cells together. I am primarily interested in cellular signals and molecular mechanisms that lead to the disruption of cellular junctions with the ultimate goal of being able to minimize effects of these stressors. I am currently using two approaches to investigate the regulation of epithelial junctional proteins. The first approach employs cellular stressors such as inflammatory mediators or hyperoxia/oxidative stress to dissect the cellular signaling events that disrupt junctions. By stressing the cell junctions I have learned about specific response and repair mechanisms. Employing specific inhibitors of various intracellular signal transduction molecules in the studies, the relative importance of individual signaling pathways contributing to junctional disruption is determined. The second approach involves using proteomics to learn about changes in cellular proteins that might contribute to the cells losing their junctions (this allows examination of what is going on inside the cells from a more global perspective). Currently, a mammalian kidney and lung model are used to study aspects of junctional physiology. Cell barrier function and viability are measured while examining changes in tight junction gene expression and protein localization within the cell following exposure to stress.

What he teaches...

Integrative Biology II is part of the introductory core sequence (Spring). My module addresses the question why do we age? We explore the facets of the biological basis of aging. Many current hypotheses concerning mechanisms of aging abound with enthusiastic research coming from cellular, invertebrate and vertebrate models. The module highlights new findings and places them in context with broader topics concerning aging. Important areas of research are presented including; free radical damage (why are antioxidants good?), molecular repair mechanisms (can you repair damage from aging?), bioenergetics (aging and “slowing down”), and hormonal regulation. As with a variety of biological processes the genetic and environmental factors that contribute to or prevent aging are discussed. Cancer rates dramatically rises with age therefore mechanisms of cancer formation are examined. In light of all the new research and anti-aging hype that bombards society, the scientific basis for these claims are explored and the synthesis of a workable model of aging is encouraged.

 

Vertebrate Physiology (Biol 3432) is a study of the principles of homeostasis with emphasis on major vertebrate organ systems. This course begins with a detailed molecular investigation of excitable membrane physiology (nerve and muscle). We then examine endocrine, cardiovascular, respiratory, renal and gastrointestinal physiology. Integrative problems are assigned to address the complex interactions between organ systems.

 

Methods in Gene Expression (Biol 2191) is designed to engage students that have completed one year of both biology and chemistry and are currently either at the sophomore or junior level. The course addresses current topics and methodologies related to eukaryotic gene expression analysis. Participants read primary scientific literature, develop a research proposal and lead discussions on relevant topics. Students are be trained on the theory and operation of several research grade instruments. There is a prominent investigational component of the course in which students are expected to conduct a series of experiments and perform the analyses to determine gene expression patterns at both the RNA and protein levels. Meeting times are spent in lecture/discussion and laboratory setting. Since the investigational laboratory is an important component of the course meets weekly for approximately three hours and occasionally at unscheduled times.

His representative publications (* indicates Trinity student) include...

  • Magazine, H.I., King, J.M. and Srivastava, K.D. Protease activated receptors modulate aortic vascular tone. International Journal of Cardiology. 1996, 53:S75-S80.
  • King, J.M., Srivastava, K.D., Stefano, G.B., Bilfinger, T.V., Bahou, W.F. and Magazine, H.I. Human monocyte adhesion is modulated by endothelin B receptor-coupled nitric oxide release. Journal of Immunology 1997,158(2) 880-886.

  • *Patrick, D.M., *Leone, A.K., *Shellenberger, J.J., *Dudowicz, K.A. and J. M. King. Proinflammatory cytokines tumor necrosis factor-α and interferon-γ modulate epithelial barrier function in Madin-Darby canine kidney cells through mitogen activated protein kinase signaling. BMC Physiology 2006, 6:2. http://www.biomedcentral.com/1472-6793/6/2

  • *Leone, A.K., *Chun, J.A., *Koehler, C.L., Caranto, J., and J.M. King. “Effect of proinflammatory cytokines tumor necrosis factor-α and interferon-γ on epithelial barrier function and matrix metalloproteinase-9 in Madin Darby Canine kidney cells.” Cellular Physiology and Biochemistry, 2007, 19:99-112.

  • Gonzalez, J.E., *Arthur, D.E., DiGeronimo, R.J., and J.M. King. Remodeling of the tight junction during recovery from exposure to hydrogen peroxide in kidney epithelial cells. Submitted to Free Radical Biology and Medicine. In review.

Selected recent conference presentations include …

  • *Leone, A.K., *Patrick, D.M., *Chun, J.A. and King, J.M. 2005. The Effects of Proinflammatory Cytokines on Matrix Metalloproteinase-9 Expression and Activity in MDCK Cells. Experimental Biology 2005 San Diego, CA. FASEB J. 19(5): 862.9.

  • *Dudowicz, K.A., *Scudder, J.D., and King, J.M. 2006. Modulation of epithelial barrier function by tumor necrosis factor-α and interferon-γ in Madin-Darby canine kidney cells is mediated through mitogen activated protein kinase signaling. Experimental Biology 2006 San Francisco, CA. FASEB J. 20(5) 687.11.

  • King, J.M., Gonzalez, J.E., *Arthur, D.E., and *D.L. Derickson. (2007). The effect of oxidative stress on the function and protein composition of tight junctions in MDCK cells. Experimental Biology, Washington D.C. FASEB J. 21:578:3.

  • *Koehler, C.L., and J.M. King. 2007. Matrix Metalloproteinase-9 targets Claudin-1 during inflammation resulting in tight junction barrier dysfunction. Cell Contact and Adhesion Gordon Research Conference, Il Ciocco, Barga, Italy. (5/31/07).

  • Gonzalez, J.E, DiGeronimo, R.J., J.M. King. (2008). Effects of oxidative stress on tight junction function and protein composition in lung epithelial cells. Southern Society for Pediatric Research. New Orleans, LA.

  • *Arthur, D.E., Gonzalez, J.E, and J.M. King. (2008). Recovery from Oxidative Stress: Effects on the Tight Junction in Epithelial Cells. Experimental Biology 2008 San Diego, CA. FASEB J. 22:758:10.

  • *Ebers, A.E., *Jenkins, J.T., *Koeher C.L., and J. M. King. (2008). Metalloproteinase Action on the Tight Junction in Epithelial Cells. Experimental Biology 2008 San Diego, CA. FASEB J. 22:1200:3.

  • King, J.M., Ribble, D.O., Elaydi, S. and J. Steele (2008). Curricula that Support Research in the Interface of Disciplines: Introductory Courses. (Interactive Session). National Conference on the Frontiers and Challenges in Undergraduate Research. College of St. Benedict, St. Joesph, MN 6/21-24/2008.

  • * Hughbanks, C.J. , * Johansen, R.M. and J.M. King (2008). The Effects of Long-Term Hyperoxia Exposure on Madin Darby Canine Kidney Cell Tight Junctions. American Society for Cell Biology 48 th Annual Meeting, San Franscico, CA.

  • * Hickey, C.J., * Koeher C.L., and J. M. King (2008). Tight Junction Protein Cleavage by Matrix Metalloproteinase-9 Results in Barrier Dysfunction. American Society for Cell Biology48 th Annual Meeting, San Franscico, CA.

Degrees...

  • B.S., Stony Brook University
  • M.A., Queens College
  • Ph.D., The Graduate Center, The City University of New York

Contact Information...

Phone number: (210) 999-7232

Email at: jking@trinity.edu

More information about his research group can be found at: http://www.trinity.edu/jking/

 

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