Mechanical stretch induces clustering of beta1-integrins and facilitates adhesion

Exp Dermatol. 2006 May;15(5):347-55. doi: 10.1111/j.0906-6705.2006.00422.x.


Human epithelial cells are permanently stimulated by external mechanical forces. The present in vitro study suggests that keratinocytes respond to mechanical strain by a coordinated spatial and functional utilization of beta1-integrins and the epidermal growth factor receptor (EGFR) with impact to the adhesion properties. It was found that a single mechanical stretch applied to HaCaT keratinocytes elevates the substrate adhesion, in particular to fibronectin and collagen type IV but not to laminin indicating the relevance of beta1-integrins in this process. This was confirmed using a functional blocking antibody directed against beta1-integrins which reversed the stretch-induced adhesion. Furthermore, mechanical stretch gives rise to a rapid redistribution of beta1-integrins in clusters on the basal cell membrane, without changing the overall amount of this particular integrin subset. Concomitantly, the EGFR co-localizes with beta1-integrin suggesting a functional cooperation of both membrane proteins in mechano-signaling. This is corroborated by data showing that stretch-induced activation of the EGFR and the downstream element extracellular regulated kinase 1/2 (ERK1/2) is reversed by preincubation with beta1-integrin antibodies. Vice versa, blocking the EGFR using a specific inhibitor abrogates stretch-induced ERK1/2 activation. In summary, these results show a functional cooperation of beta1-integrins and EGFR in the adhesion complex supporting the transmission of stretch-induced signals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion
  • Cell Line
  • ErbB Receptors / metabolism*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Integrin beta1 / metabolism*
  • Keratinocytes / metabolism
  • Keratinocytes / physiology*
  • Microscopy, Confocal
  • Stress, Mechanical


  • Integrin beta1
  • ErbB Receptors
  • Extracellular Signal-Regulated MAP Kinases