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Ji Ming Wang, M.D., Ph.D.

Laboratory of Molecular Immunoregulation Head, Chemoattractant Receptor and Signal Group Senior Investigator Building 560, Room 31-68 NCI-Frederick Frederick, MD 21702-1201 Phone:   301-846-6979 Fax:   301-846-7042 E-Mail:   wangji@mail.ncifcrf.gov

Biography

Dr. Ji Ming Wang, head of the Chemoattractant Receptor and Signal Group, is engaged in studies on the role of chemoattractant receptors in host defense against HIV-1 infection and the pathogenesis of neurodegenerative diseases.

Research

The Role of Chemoattractants and Receptors in Host Defense

Chemoattractant receptors are seven-transmembrane (STM), G-protein coupled receptors, which mediate leukocyte trafficking by recognizing exogenous or host derived chemotactic factors. A variety of malignant tumor cells of the non-leukocyte lineage also express some of such receptors. Dr. Wang's laboratory has found that these receptors, when activated by agonists, increased the capability of tumor cells to proliferate, to produce angiogenic factors and to metastasize to distant organs. Therefore, these receptors constitute a group of important molecular targets for better understanding the mechanisms that control the progression of malignant tumors and for the development of novel anti-cancer agents.

Dr. Wang's studies have been expanded to the role of chemoattractant receptors in the pathogenesis of neurodegenerative diseases. Abeta42 is a 42 amino acid form of the beta amyloid peptide and is a key causative factor of Alzheimer's disease (AD). In addition to its reported direct toxic effect on nerve cells, Abeta42 has been found to activate mononuclear phagocytic cells in the brain and causes inflammation and release of neurotoxic mediators. Dr. Wang's group has identified a STM receptor, FPRL1, to be used by Abeta42 to induce mononuclear phagocyte migration and activation. In addition, they detected a high level of expression of the FPRL1 gene in CD11b positive phagocytic cells surrounding and infiltrating the lesions in the brain tissues of AD patients. These results suggest an active involvement of this receptor in the proinflammatory aspects of AD lesions. Interestingly, recent research by this group also revealed FPRL1 to be a receptor for a peptide fragment of the human prion protein, which, in its isoforms, causes 'Kuru' or 'Mad Cow' disease. The peptide fragment Prp10-126 forms aggregates and activates mononuclear phagocytes to release mediators toxic to neurons in vitro. Studies are being conducted to elucidate the role of FPRL1 in the pathogenesis of neurodegenerative diseases and its potential as a therapeutic target.

This page was last updated on 6/12/2008.