Enhancement of ectopic bone formation in mice with a deficit in Fas- mediated apoptosis

Shiro Mori, Masato Nose, Masatoshi Chiba, Kenji Narita, Masahiro Kumagai, Hiromi Kosaka, Teiichi Teshima

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Bone formation is under the control of cytokines as well as growth factors such as bone morphogenetic proteins (BMP). This suggests the possibility that osteogenesis might be modulated by factors which also modulate the immune system. To test whether immune disorders in the host may influence bone formation, we studied BMP-induced bone formation in a C3H/HeJ strain of mice bearing a mutant gene, the lymphoproliferation gene (lpr) or the generalized lymphoproliferative disease gene (gld), both of which are known to be a Fas deletion mutant and a Fas ligand mutant, respectively, and to induce immune disorders via a deficit in Fas-mediated apoptosis. Crude BMP derived from bovine bone were injected into the muscular tissue in the femur of adult C3H/HeJ mice or C3H/HeJ mice bearing an lpr or gld gene. Quantitative analysis of the resulting ectopic bone formation by X-ray photography 2 weeks after injection revealed that the presence of either the lpr or gld gene caused a bone mass significantly larger in dimension than that seen in the wild type mice. Histological examination also revealed the different influence between these mutant genes on the level of bone formation exhibited by hyaline cartilage and bone trabeculae. Based on these results, we discussed the possible mechanisms of the enhanced ectopic bone formation under the deficit in Fas-mediated apoptosis.

Original languageEnglish
Pages (from-to)112-116
Number of pages5
JournalPathology international
Volume47
Issue number2-3
DOIs
Publication statusPublished - 1997

Keywords

  • Fas
  • Fas ligand
  • apoptosis
  • bone morphogenetic proteins
  • ectopic bone formation

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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