Absence of transcription factor c-maf causes abnormal terminal differentiation of hypertrophic chondrocytes during endochondral bone development
pmid: 14512017
Absence of transcription factor c-maf causes abnormal terminal differentiation of hypertrophic chondrocytes during endochondral bone development
In this study, we report that the transcription factor c-Maf is required for normal chondrocyte differentiation during endochondral bone development. c-maf is expressed in hypertrophic chondrocytes during fetal development (E14.5-E18.5), with maximal expression in the tibia occurring at E15.5 and E16.5, in terminally differentiated chondrocytes. In c-maf-null mice, fetal bone length is decreased approximately 10%, and hypertrophic chondrocyte differentiation is perturbed. There is an initial decrease in the number of mature hypertrophic chondrocytes at E15.5 in c-maf-null tibiae, with decreased expression domains of collagen X and osteopontin, markers of hypertrophic and terminal hypertrophic chondrocytes, respectively. By E16.5, there is an expanded domain of late hypertrophic, osteopontin-positive chondrocytes in the c-maf-/-. This accumulation of hypertrophic chondrocytes persists and is still observed at 4 weeks of age. These data suggest that c-Maf facilitates the initial chondrocyte terminal differentiation and influences the disappearance of hypertrophic chondrocytes. BrdU and TUNEL analyses show normal proliferation rate and apoptosis in the c-maf-null. There is a specific decrease in MMP-13 expression at E15.5 in the c-maf-null. MMP-13 is known to be regulated by AP-1 and may also be a target of c-Maf. Thus, cartilage is a novel system in which c-Maf acts during development, where c-Maf is required for normal chondrocyte differentiation.
- Massachussetts General Hospital Harvard Medical School Neurogenetics Unit United States
- University of Melbourne Australia
- Boston Children's Hospital United States
- Harvard University United States
c-maf, Apoptosis, Ossification, Mice, Chondrocytes, Proto-Oncogene Proteins, Matrix Metalloproteinase 13, Animals, Collagenases, Molecular Biology, Mice, Inbred BALB C, Bone Development, Osteoblasts, Cell Differentiation, Cell Biology, Hypertrophy, Chondrocyte, Vascular invasion, DNA-Binding Proteins, Cartilage, Differentiation, Proto-Oncogene Proteins c-maf, MMP-13, Tumor Suppressor Protein p53, Cell Division, Developmental Biology
c-maf, Apoptosis, Ossification, Mice, Chondrocytes, Proto-Oncogene Proteins, Matrix Metalloproteinase 13, Animals, Collagenases, Molecular Biology, Mice, Inbred BALB C, Bone Development, Osteoblasts, Cell Differentiation, Cell Biology, Hypertrophy, Chondrocyte, Vascular invasion, DNA-Binding Proteins, Cartilage, Differentiation, Proto-Oncogene Proteins c-maf, MMP-13, Tumor Suppressor Protein p53, Cell Division, Developmental Biology
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