Mouse cathepsin K: cDNA cloning and predominant expression of the gene in osteoclasts, and in some hypertrophying chondrocytes during mouse development
Authors:
- Hannu T. AroHAHannu T. Aro
- Mikko SavontausMSMikko Savontaus
- Eero VuorioEVEero Vuorio
- 16 September 1996
- journal article
- Published by Wiley in FEBS Letters
- Vol. 393 (2-3) , 307-313
Abstract
We have constructed cDNA clones covering the entire coding region of mouse, human and rabbit preprocathepsin K mRNA for studies on bone turnover. The clone pMCatK‐1 for mouse cathepsin K shares 87% nucleotide homology with the corresponding human and rabbit sequences. Analysis of a panel of mouse tissues for tissue distribution of cathepsin K mRNA revealed the highest levels in musculoskeletal tissues: bone, cartilage and skeletal muscle. In situ hybridization of developing mouse embryos was performed to identify the cellular source of cathepsin K mRNA. The strongest mRNA signal was detected in osteoclasts of bone, identified in serial sections by positive TRAP staining. Cathepsin K mRNA was also observed in some hypertrophic chondrocytes of growth cartilages. Association of cathepsin K production with degradation of bone and cartilage matrix suggests that this enzyme and its mRNA levels could serve as markers for matrix degradation in diseases affecting these tissues.Keywords
This publication has 23 references indexed in Scilit:
- Increased expression of TGF-beta 2 in osteoblasts results in an osteoporosis-like phenotype.Journal of Cell Biology, 1996
- Molecular cloning of human cathepsin O, a novel endoproteinase and homologue of rabbit OC2FEBS Letters, 1995
- Human Cathepsin O2, a Novel Cysteine Protease Highly Expressed in Osteoclastomas and Ovary Molecular Cloning, Sequencing and Tissue DistributionBiological Chemistry Hoppe-Seyler, 1995
- Molecular Cloning of Human cDNA for Cathepsin K: Novel Cysteine Proteinase Predominantly Expressed in BoneBiochemical and Biophysical Research Communications, 1995
- Retarded chondrogenesis in transgenic mice with a type II collagen defect results in fracture healing abnormalitiesDevelopmental Dynamics, 1994
- High expression of 92-kD type IV collagenase (gelatinase B) in the osteoclast lineage during mouse developmentJournal of Cell Biology, 1994
- Mechanism of Bone TurnoverAnnals of Medicine, 1993
- Bone and haematopoietic defects in mice lacking c-fosNature, 1992
- Local and Systemic Factors in the Pathogenesis of OsteoporosisNew England Journal of Medicine, 1988
- Isolation of biologically active ribonucleic acid from sources enriched in ribonucleaseBiochemistry, 1979