Absence of transcription factor c-maf causes abnormal terminal differentiation of hypertrophic chondrocytes during endochondral bone development

Dev Biol. 2003 Oct 1;262(1):51-63. doi: 10.1016/s0012-1606(03)00324-5.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis
  • Bone Development / physiology*
  • Cell Differentiation / physiology*
  • Cell Division
  • Chondrocytes / cytology*
  • Collagenases / genetics
  • DNA-Binding Proteins / physiology*
  • Hypertrophy
  • Matrix Metalloproteinase 13
  • Mice
  • Mice, Inbred BALB C
  • Osteoblasts / physiology
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-maf
  • Tumor Suppressor Protein p53 / analysis

Substances

  • DNA-Binding Proteins
  • Maf protein, mouse
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-maf
  • Tumor Suppressor Protein p53
  • Collagenases
  • Matrix Metalloproteinase 13
  • Mmp13 protein, mouse