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Faculty Detail    
Name WEI CHEN
 
Campus Address SHEL 815 Zip 0007
Phone 205-975-2607
E-mail wechen@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Associate Professor

Graduate Biomedical Sciences Affiliations
Molecular and Cellular Pathology Program 

Biographical Sketch 
Dr. Wei Chen is Associate Professor in the Department of Pathology at The University of Alabama at Birmingham. Before joining UAB, Dr. Chen was instructor of Oral Biology Department, Harvard School of Dental Medicine and Associate Research Investigator (equivalent to Research Associate Professor) in the Department of Cytokine Biology, at the Forsyth Institute, Harvard School of Dental Medicine. Dr. Chen received her M.D. in 1983 at the Kunming Medical College in China. Dr. Chen received her postdoctoral research training at the Forsyth Institute, Harvard School of Dental Medicine.

Society Memberships
Organization Name Position Held Org Link
American Society for Bone and Mineral Research  Member  www.asbmr.org 
International Association for Biological and Medical Research  Member  www.IABMR.org 

Research/Clinical Interest
Title
Understanding the mechanisms of bone formation, bone resorption, skeletal development, craniofacial development and cancer bone metastasis; Developing effective new therapies for treating and preventing the related diseases.
Description
1. To reveal the mechanisms underlying the transcription factors that regulates osteoclast lineage commitment, differentiation, and function. We have determined the essential role of a number of transcription factors, eg. AML-1 and C/EBP alpha, in dose dependent osteoclast lineage commitment, differentiation, activation, and function. 2. To elucidate the mechanism of bone resoprtion. This consists of investigating the role of subunits of the osteoclast proton pump (SOPP) in osteoclast functions (e.g., osteoclast-mediated extracellular acidification, membrane trafficking, exocytosis) and elucidating their potential role in developing a means to cure or alleviate human osteolytic diseases. Previously, we showed that inactivation of subunit a3 (also known as ATP6V0A3 or TCIRG1) leads to osteopetrosis in mice because of nonfunctional osteoclasts that are incapable of acidifying the extracellular resorption lacuna. 3. To elucidate the mechanism of bone formation and develop a means to cure or alleviate bone abnormalities, such as osteoporosis. Attractive targets are osteoblast cells, which increase bone formation. Our previous work shows that cellular nucleic acid binding protein (CNBP) is expressed in all stages of osteoblast lineage. Furthermore, we have demonstrated that CNBP is located in both the nucleus and the cytoplasm, which indicates that it may be a dual regulator of transcription and translation. 4. To identify how cellular nucleic acid binding protein (CNBP) and other transcription factors regulate craniofacial development and disease and to expand our understanding of the biological and molecular basis of craniofacial morphogenesis. We have characterized the functions of CNBP in head formation in chicken and mouse models through gene knockout misexpression and tissue-specific targeted disruption approaches (Development, 2003; Developmental Biology, 2006). 5. To define the role of Znf9 in myotonic dystrophy type 2 (DM2) and muscle development. We characterized Znf9+/- mice and found that their phenotype reflects many of the features in myotonic dystrophy. Znf9 is highly expressed in skeletal and heart muscle. Our data demonstrated that Znf9 haploinsufficiency might contribute to the myotonic dystrophy phenotype in Znf9+/- mice (J. Molecular Biology, 2007). 6. To discover and develop a novel anti-cancer drug---vascular disrupting agents (VDAs) that selectively targets tumor vessels, harbored significant anti-vascular capabilities and minimal toxic side-effects. We have identified a remarkable new drug that powerfully acts against tumors, while circumventing the difficulties and adverse effects of conventional antitumor treatments. We are currently developing this drug and investigating the molecular mechanism of its antitumor effects.

Selected Publications 
Publication PUBMEDID
Chen W, Li Y-P. Generation of mouse osteoclastogenic cell lines immortalized with SV-40 large T antigen. J Bone Miner Res 1998;13:1112-23.   9661075 
*Chen W, Zhu G, Hao L, Wu M, Ci HL, and Li YP. C/EBPa is the Key Regulator of Osteoclast Lineage Commitment. Proc Natl Acad Sci U S A. PNAS 2013 ; published ahead of print   23580622  
Jiang HB*, Chen W*,#,, Zhu G, Zhang L, Tucker B, Hao L, Feng S, Ci H, Ma J, Wang L, Stashenko P, and Li Y-P. RNAi-Mediated Silencing of Atp6i and Atp6i Haploinsufficiency Prevents Both Bone Loss and Inflammation in a Mouse Model of Periodontal Disease. PLOS ONE. 2013;8(4):e58599. *authors contributed equally as first authors, #Co-correspondence author.  23577057  
Ma, J*, Chen W*,#, Zhang L, Tucker B, Zhu G, Sasaki H, Hao L, Wang L, Ci H, Jiang H, Stashenko P, and Li Y-P#. RNAi mediated silencing of Atp6i prevents both periapical bone erosion and periapical inflammation in the mouse model of endodontic disease. Infection and Immunity. 2013; 81 (4): 1021–1030. *authors contributed equally as first authors, #Co-correspondence author.
 
23166162 
Bo Gao*, Chen W*,#, Liang Hao, Guochun Zhu, Shengmei Feng, Hongliang Ci, Xuedong Zhou, Philip Stashenko and Li Y-P#. Inhibiting periapical lesions through AAV-RNAi silencing of Cathepsin K. J Dent Res 2013; 92 (2): 180 - 186. *authors contributed equally as first authors, #Co-correspondence author.  23166044 
Wu M, Wang Y, Deng LF, Chen W, Li Y-P. TRAF Family Member-Associated NF-κB Activator (TANK) Induced By RANKL Negatively Regulates Osteoclasts Survival and Function. Int J Biol Sci 2012; 8(10):1398-1407.   23139637 
Yang DQ, Feng S, Chen W, Zhao H, Paulson C, Li YP. V-ATPase subunit ATP6AP1 (Ac45) regulates osteoclast differentiation, extracellular acidification, lysosomal trafficking, and protease exocytosis in osteoclast-mediated bone resorption. J Bone Miner Res. 2012 Aug;27(8):1695-707.   22467241 
Horst D, Gu X, Bhasin M, Yang Q, Verzi M, Lin D, Joseph M, Zhang X, Chen W, Li Y-P, Shivdasani1 RA, Libermann TA. Requirement of the Epithelial-Specific Ets Transcription Factor Spdef for Mucous Gland Cell Function in the Gastric Antrum. J Biol Chem 2010; 285:35047-35055.   20801882 
Soltanoff CS, Chen W, Yang S, Li Y-P. The signaling networks that control the lineage commitment and differentiation of bone cells. Crit Rev Eukaryot Gene Exp. 2009; 19:1-46.   19191755 
Feng M, Deng , Chen W, Shao J, Xu G, Li Y-P. Atp6v1c1 is an essential component of the osteoclast proton pump and in F-actin ring formation in osteoclast. Biochemistry J 2009; 417:195-205.   18657050 
Yang S, Chen W, Stashenko P, Li Y-P. Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation. J Cell Sci 2007;120:3362-71.   17881498 
Chen W, Wang Y, Abe Y, Cheney L, Udd B, Li Y-P. Haploinsuffciency for Znf9 in Znf9+/- mice is associated with multiorgan abnormalities resembling myotonic dystrophy. J Mol Biol 2007;368:8-17.   17335846 
Chen W, Yang S, Abe Y, Li M, Wang Y, Shao J, Li E, Li Y-P. Novel pycnodysostosis mouse model uncovers cathepsin K function as a potential regulator of osteoclast apoptosis and senescence. Hum Mol Genet 2007;16:410-23.  17210673 
Zhao Q, Shao J, Chen W, Li Y-P. Osteoclast differentiation and gene regulation. Frontiers Biosci 2007;12:2519-29.  17127260 
Abe Y, Chen W*, Huang W, Li Y-P. CNBP regulates forebrain formation at organogenesis stage in chick embryos. Dev Biol 2006;295:116-27. * Equal contribution  16626683 
Kamolmatyakul S, Chen W, Li Y-P. Interferon-Gamma; down-regulates gene expression of cathepsin K in osteoclasts and inhibits osteoclast formation. J Dent Res 2001;80:351-5.   15381721 
Shimizu K, Chen W, Ashique AM, Moroi R, Li Y-P. Molecular cloning, developmental expression, promoter analysis and functional characterization of the mouse CNBP gene. Gene 2003;307:51-62.   12706888 
Chen W, Liang Y, Deng W, Shimizu K, Ashique AM, Li E, Li Y-P. The zinc-finger protein, CNBP, is required for forebrain formation in the mouse. Development 2003;130:1367-79.   12588852 
Deng W, Stashenko P, Chen W, Liang Y, Shimizu K, Li Y-P. Characterization of mouse Atp6i gene, the gene promoter, and the gene expression. J Bone Miner Res 2001;16:1136-46.  11393791 
Li Y-P, Chen W, Liang Y, Li E, Stashenko P. Atp6i-deficient mice exhibit severe osteopetrosis due to loss of osteoclast-mediated extracellular acidification. Nat Genet 1999;23:447-451.  10581033 
Li Y-P, Chen W. Characterization of mouse cathepsin K gene, the gene promoter, and the gene expression. J Bone Miner Res 1999;14:487-99.   10234569 

Keywords
Muscular development, Osteoclasts and Osteoblasts, Bone formation and bone resorption, Skeletal development, Tumorigenesis, Cancer bone metastasis, Brain and craniofacial development, and related diseases, as well as Anti-cancer drug discovery.