Erk pathways negatively regulate matrix mineralization

Shin jiro Kono, Yasushi Oshima, Kazuto Hoshi, Lynda F. Bonewald, Hiromi Oda, Kozo Nakamura, Hiroshi Kawaguchi, Sakae Tanaka

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Skeletal mineralization is an important step regulating the mechanical properties of the calcified tissues, but molecular events underlying mineralization still remain elusive. We examined the role of extracellular signal-regulated kinase (Erk) pathways in matrix mineralization of osteogenic cells both in vitro and in vivo. Matrix mineralization by preosteocytic MLO-A5 cells and osteoblastic MC3T3-E1 cells was increased by either PD98059 Mek inhibitor treatment or adenovirus vector-mediated dominant negative Ras (RasDN) expression and was suppressed by Erk activation by platelet-derived growth factor (PDGF) treatment or constitutively active Mek1 (MekCA) expression. Administration of adenovirus vectors carrying RasDN gene onto the calvaria of 1-day-old mice increased the mineralization of the tissues, while that of the MekCA adenovirus suppressed it. These results suggest that the Erk pathway is a negative regulator of the matrix mineralization both in vitro and in vivo.

Original languageEnglish (US)
Pages (from-to)68-74
Number of pages7
Issue number1
StatePublished - Jan 2007
Externally publishedYes


  • Erk
  • Mek
  • Mineralization
  • Osteoblast
  • Osteocyte
  • Ras

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Histology

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