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Faculty

Suil Kim, M.D., Ph.D.
Assistant Professor of Medicine


University of California San Francisco
Cardiovascular Research Institute
505 Parnassus Avenue, Box 0130
San Francisco, California 94143-0130

phone: 415-476-2962
fax: 415-476-2283
email: suil.kim@ucsf.edu


Dr. Kim received his AB in Chemistry and SM in Biochemistry from the Univ. of Chicago. He received his MD and PhD degrees from the Univ. of Michigan in 1996 and completed residency training in Internal Medicine at the Univ. of Pittsburgh. Moving west, he completed fellowship training in Pulmonary and Critical Care Medicine at the Univ. of California San Francisco. After research training with Dr. Jay Nadel in the Cardiovascular Research Institute, Dr. Kim joined the pulmonary faculty in 2004. His major academic activities include basic research and clinical medicine as an attending physician at the San Francisco VA Medical Center.

Research Interests

The two lung diseases that contribute most to human morbidity and mortality worldwide are chronic obstructive pulmonary disease (COPD) and lung adenocarcinoma. Currently, there are no effective medical therapies for either disease. In chronic inflammatory airway diseases such as COPD, excess mucus plugs the airways, impairs mucociliary clearance, and promotes inflammation caused by inhaled materials. Our lab discovered that epidermal growth factor receptor (EGFR) activation causes mucin production in airway epithelial cells in vivo and in vitro. Subsequently, EGFR activation has been implicated in mucin upregulation by many stimuli including bacteria, viruses, allergens, cigarette smoke, mechanical irritants, reactive oxygen species, cytokines, and activated leukocytes, suggesting that the EGFR cascade is a convergent pathway for mucin production by multiple stimuli in airway epithelial (goblet) cells. Present evidence suggests that goblet cells arise via EGFR-mediated cell differentiation. Conversely, EGFR activation is also implicated in the uncontrolled proliferation, resistance to apoptosis, and metastasis of lung adenocarcinoma cells. Therefore, the EGFR cascade is a rational target for treatment of both mucus hypersecretion and lung adenocarcinoma.

My research program focuses on characterizing the mechanisms that lead to diverse biological responses to EGFR activation in airway epithelium and identifying potential therapeutic targets in the EGFR signaling pathway. I am interested in how the local environment of airway epithelial cells, in particular cell-cell and cell-substrate interactions, modulates EGFR signaling to produce divergent cell outcomes such as differentiation (mucin production) and proliferation. To examine these interactions I utilize clinically relevant animal models, ex vivo airway epithelium, and cultured human airway epithelial cells. The characterization of signals that influence the outcome of EGFR activation will increase our understanding of the mechanisms involved in mucus hypersecretion and lung adenocarcinoma and may lead to rational therapies for these diseases.

Selected Publications


Lee H-M, Malm L, Dabbagh K, Dao-Pick T, Ueki IF, Kim S, Shim JJ, and Nadel JA (2001). EGFR signaling mediates regranulation of nasal goblet cells. J Allergy Clin Immunol 107: 1046-1050.

Kim S, Gotway M, Webb WR, Gordon R, and Golden J (2002). Tracheal compression by the stomach following gastric pull-up: diagnosis with CT and treatment with expandable metallic stent placement. Chest 121: 998-1001.

Kim S, Shim JJ, Burgel P-R, Ueki I, Dao-Pick T, Tam D, and Nadel JA (2002). IL-13-induced CCSP expression in airway epithelium: role of EGF-R signaling pathway. Am J Physiol Lung Cell Mol Physiol 283: L67-75.

Kim S, and Nadel JA (2004). Role of neutrophils in mucus hypersecretion in COPD and implications for therapy. Treat Respir Med 3: 147-159.

Kim S, Shao MX-G, and Nadel JA (2005). Mucus production, secretion, and clearance. In: Mason RJ, Broaddus VC, Murray JF, Nadel JA, editors. Textbook of Respiratory Medicine, 4th ed., Philadelphia, Saunders, pp 330-354.

Kim S, Schein AJ, and Nadel JA (2005). E-cadherin promotes EGFR-mediated cell differentiation and MUC5AC mucin expression in cultured human airway epithelial cells. Am J Physiol Lung Cell Mol Physiol 289: L1049-1060.

Koff, JL, Shao, M, Kim, S, Ueki, IF, and Nadel, JA (2006).  Pseudomonas LPS accelerates wound repair via activation of a novel epithelial cell signaling cascade. J Immunol 177: 8693-8700.


Last Update: 2/21/08

     
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