Abstract

The matrix proteins of bones and teeth play key roles in the structure and function of these tissues. Our objective is to study the structure and function of these macromolecules and to understand the regulation of their expression. The structures of bone and tooth matrix proteins have been studied by constructing recombinant cDNA libraries from bone or ameloblast cell mRNA. cDNAs encoding several bone and tooth matrix proteins were isolated using expression vectors and mono-specific antisera directed against individual bone and ameloblast proteins were produced. The clones and antibodies were used to determine the primary structure and mode of expression of the genes in cultured cells and intact tissue. The corresponding genomic DNAs have also been isolated and used to determine the intron-exon organization of these genes and the elements that potentially regulate their expression during development. Studies are underway using transgenic mice to identify the function of the matrix proteins and the elements that regulate their expression during development and aging in vivo.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Intramural Research (Z01)
Project #
1Z01DE000379-09
Application #
3839197
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
9
Fiscal Year
1992
Total Cost
Indirect Cost

  Institution

Name
National Institute of Dental & Craniofacial Research
Department
Type
DUNS #
City
State
Country
United States
Zip Code

  Publications

Ono, Mitsuaki; Masaki, Asuka; Maeda, Azusa et al. (2018) CCN4/WISP1 controls cutaneous wound healing by modulating proliferation, migration and ECM expression in dermal fibroblasts via ?5?1 and TNF?. Matrix Biol 68-69:533-546
Kram, Vardit; Kilts, Tina M; Bhattacharyya, Nisan et al. (2017) Small leucine rich proteoglycans, a novel link to osteoclastogenesis. Sci Rep 7:12627
Maeda, Azusa; Ono, Mitsuaki; Holmbeck, Kenn et al. (2015) WNT1-induced Secreted Protein-1 (WISP1), a Novel Regulator of Bone Turnover and Wnt Signaling. J Biol Chem 290:14004-18
Babelova, Andrea; Moreth, Kristin; Tsalastra-Greul, Wasiliki et al. (2009) Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. J Biol Chem 284:24035-48
Wallace, Joseph M; Rajachar, Rupak M; Allen, Matthew R et al. (2007) Exercise-induced changes in the cortical bone of growing mice are bone- and gender-specific. Bone 40:1120-7
Heegaard, Anne-Marie; Corsi, Alessandro; Danielsen, Carl Christian et al. (2007) Biglycan deficiency causes spontaneous aortic dissection and rupture in mice. Circulation 115:2731-8
Wadhwa, Sunil; Bi, Yanming; Ortiz, Ana T et al. (2007) Impaired posterior frontal sutural fusion in the biglycan/decorin double deficient mice. Bone 40:861-6
Bi, Yanming; Ehirchiou, Driss; Kilts, Tina M et al. (2007) Identification of tendon stem/progenitor cells and the role of the extracellular matrix in their niche. Nat Med 13:1219-27
Goldberg, Michel; Septier, Dominique; Oldberg, Ake et al. (2006) Fibromodulin-deficient mice display impaired collagen fibrillogenesis in predentin as well as altered dentin mineralization and enamel formation. J Histochem Cytochem 54:525-37
Wallace, Joseph M; Rajachar, Rupak M; Chen, Xiao-Dong et al. (2006) The mechanical phenotype of biglycan-deficient mice is bone- and gender-specific. Bone 39:106-16

Showing the most recent 10 out of 51 publications