Betaig-h3 supports keratinocyte adhesion, migration, and proliferation through alpha3beta1 integrin

Biochem Biophys Res Commun. 2002 Jun 28;294(5):940-8. doi: 10.1016/S0006-291X(02)00576-4.


betaig-h3 is an extracellular matrix protein and its expression is highly induced by TGF-beta and it has also been suggested to play important roles in skin wound healing. In this paper, we demonstrate that betaig-h3 is present in the papillary layer of dermis and synthesized in the basal keratinocytes in vivo and its expression is induced by TGF-beta in normal human keratinocytes (NHEK) and HaCaT cells. betaig-h3 mediates not only adhesion and spreading of keratinocytes but also supports migration and proliferation. These activities are mediated through interacting with alpha3beta1 integrin. Previously identified two alpha3beta1 integrin-interacting motifs of betaig-h3, EPDIM, and NKDIL, are responsible for these activities. The results suggest that betaig-h3 may regulate keratinocyte functions in normal skin and potentially during wound-healing process.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Cell Adhesion*
  • Cell Division
  • Cell Line
  • Cell Movement*
  • Cells, Cultured
  • Conserved Sequence
  • Dermis / anatomy & histology
  • Dermis / chemistry
  • Extracellular Matrix Proteins*
  • Humans
  • Integrin alpha3beta1
  • Integrins / physiology*
  • Keratinocytes / cytology
  • Keratinocytes / drug effects
  • Keratinocytes / physiology*
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / chemistry
  • Neoplasm Proteins / pharmacology*
  • Peptides / chemistry
  • Peptides / pharmacology
  • Skin / cytology
  • Transforming Growth Factor beta / pharmacology


  • Extracellular Matrix Proteins
  • Integrin alpha3beta1
  • Integrins
  • Neoplasm Proteins
  • Peptides
  • Transforming Growth Factor beta
  • betaIG-H3 protein