Enhanced c-Fms/M-CSF receptor signaling and wound-healing process in bone marrow-derived macrophages of signal-transducing adaptor protein-2 (STAP-2) deficient mice

Osamu Ikeda, Yuichi Sekine, Ryuta Muromoto, Norihiko Ohbayashi, Akihiko Yoshimura, Tadashi Matsuda

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Signal-transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein as a c-Fms/M-CSF receptor-interacting protein and constitutively expressed in macrophages. In our previous study, we examined the role of STAP-2 in the c-Fms/M-CSF receptor signaling using a murine macrophage tumor cells line, Raw264.7. Overexpression of STAP-2 in Raw264.7 cells markedly suppressed M-CSF-induced activation of extracellular signal regulated kinase and Akt. In addition, Raw264.7 overexpressing STAP-2 affected cell migration in wound-healing process. These results suggest that STAP-2 deficiency influences endogenous c-Fms/M-CSF receptor signaling. Here we show that loss of STAP-2 expression in knockout mouse macrophages results in marked enhancement of the c-Fms/M-CSF receptor signaling and wound-healing process. We therefore propose that STAP-2 acts as an endogenous regulator in normal macrophages functions.

Original languageEnglish
Pages (from-to)1790-1793
Number of pages4
JournalBiological and Pharmaceutical Bulletin
Volume31
Issue number9
DOIs
Publication statusPublished - 2008 Sep
Externally publishedYes

Keywords

  • C-Fms
  • M-CSF
  • Macrophage
  • Signal-transducing adaptor protein-2
  • Wound-healing

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

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