Dr. Kim

Kwang Chul Kim, Ph.D.

Professor of Pharmacy and Medicine

Department: Division
Medicine: Pulmonary and Critical Care Medicine

  • PhD - Ohio State University, Ph.D. in Pharmacology (1979)
  • National Institute of Environmental Health Sciences, NIH (80-83)
  • W. Alton Jones Cell Science Center (84)
  • Professor of Pharmacy and Medicine

Current Research Interests:

  • Role of MUC1 mucin in airway defense
  • Role of MUC1 mucin in lung injury and repair
  • Transcriptional regulation of MUC1 gene
  • Elucidation of MUC1 Signaling pathway
  • Role of airway mucus in normal physiology and pathology
  • Pharmacology of airway mucus secretion
  • Development of a drug to control airway mucus hypersecretion

Dr. Kim's major area of research is the cell biology of airway mucus glycoprotein, a major component of mucus, which is responsible for the physicochemical property of mucus. He was a pioneer in the area of airway mucin pharmacology through development and characterization of airway cell culture systems from various animals during his postdoctoral years at NIH. During his junior faculty years in Boston, he discovered two important endogenous agents that stimulate airway mucin secretion ”“ neutrophil elastase and ATP. These are the two most potent agents among all the agents, exogenous or endogenous, that have been reported. While working on the mechanism of neutrophil elastase induced mucin release, he discovered that the mucins released by elastase are derived from the cell surface. It was the first report showing the presence of a cell surface mucin, which turned out to be MUC1 mucin. Since his move to University of Maryland, he has been focusing mainly on the structure and function of airway MUC1 mucin.

Recently, he found that MUC1 mucin is an adhesion site for Pseudomonas aeruginosa and that the binding involves flagella. Furthermore, some of his preliminary results indicated that the interaction of flagellin with MUC1 on the cell surface induces phosphorylation of MUC1 in its cytoplasmic domain, suggesting that MUC1 is likely a receptor of Pseudomonas aeruginosa and should play an important role during airway infection. This new finding had a major impact in our current understanding of how the bacteria interact with airway surface epithelium in cystic fibrosis. Given the presence of multiple signaling motifs on the cytoplasmic domain of MUC1, there seems to be no doubt that this molecule plays a very important role in the airway function. In addition, he has a patent on a peptide that has an ability to suppress airway mucus hypersecretion.

Current Research Funding

2000 ”“ 2004

NIH RO1 HL-63742 (PI)
“A novel negative regulatory element in the MUC1 promoter”
2001 ”“ 2004

Cystic Fibrosis Foundation (PI)
“Role of MUC1 mucin in Pseudomonas infection”
2001 ”“ 2005

NIH RO1 HL-47125 (PI)
“the signaling mechanism of MUC1 mucin”
2001 - 2003

Maryland Industrial Partnerships Fund (MIPS)
“Development of airway mucous secretion inhibitors”
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