Position

Assistant Professor

Education

Ph.D., Graduate Institute of Medical Sciences, National Defense Medical Center, ROC

M.S., Graduate Institute of Microbiology and Immunology, National Defense Medical Center, ROC

B.S., Department of Public Health, National Defense Medical Center, ROC

Interests

1. Investigations on the pathogenesis and molecular mechanism in autoimmune diseases especially in rheumatoid arthritis.

2. Investigations on the molecular factors in osteoclastogenesis and osteoporosis.

Email

ph870317@ndmctsgh.edu.tw

Publications

1. Cheng CP, Sheu MJ, Sytwu HK, Chang DM. Decoy receptor 3 suppresses RANKL-induced osteoclastogenesis via down-regulating NFATc1 and enhancing cell apoptosis. Rheumatology (Oxford). 2013 Apr;52(4):609-22. (SCI, 2012 IF=4.212, Ranking:7/29)

2. Cheng CP, Sytwu HK, Chang DM. Decoy receptor 3 attenuates collagen-induced arthritis by modulating T cell activation and B cell expansion. J Rheumatol. 2011 Dec; 38(12):2522-35. (SCI, 2011 IF=3.695 Ranking:11/29)

3. Cheng CP, Huang HS, Hsu YC, Sheu MJ, Chang DM. A benzamide-linked small molecule NDMC101 inhibits NFATc1 and NF-κB activity: a potential osteoclastogenesis inhibitor for experimental arthritis. J Clin Immunol. 2012 Aug;32(4):762-77. (SCI, 2012 IF=3.382 Ranking:55/137)

4. Hsu YC, Cheng CP, Chang DM. Plectranthus amboinicus attenuates inflammatory bone erosion in mice with collagen-induced arthritis by downregulation of RANKL-induced NFATc1 expression. J Rheumatol. 2011 Sep;38(9):1844-57. (SCI, 2011 IF=3.695 Ranking:11/29)

Laboratory Description

Our laboratory is interested in the development of irregular immune system in autoimmune disease and bone remodeling system. We try to find out the aberrantly expressing disease-related gene to become a therapeutic target. Also, we try to figure out the effect and molecule mechanisms of candidate gene in the development of immune system in disease progress.

Our previous studies are focused on the role of human specific gene, decoy receptor 3 (DCR3) in rheumatoid arthritis. We found that over expressing DCR3 gene could attenuate disease severity in a mouse model (collagen-induced arthritis, CIA) of rheumatoid arthritis. Also, the immune system of this disease especially in B and T lymphocytes seems to be unaffected by this kind of manipulation in CIA mice. Furthermore, we found normal osteoclast differentiation would be enforced to death after DCR3 highly expressing. One of it’s ligands, Fas ligand which was related to cell apoptosis was also highly expressed. Moreover, the intrinsic apoptosis signal of these osteoclasts, like caspase 9, cytochrome c, etc. would be up-regulated. These evidences may help us to realize the real role of human specific gene in human autoimmune disease.