Gingival fibroblasts display reduced adhesion and spreading on extracellular matrix: a possible basis for scarless tissue repair?

PLoS One. 2011;6(11):e27097. doi: 10.1371/journal.pone.0027097. Epub 2011 Nov 2.

Abstract

Unlike skin, oral gingiva do not scar in response to injury. The basis of this difference is likely to be revealed by comparing the responses of dermal and gingival fibroblasts to fibrogenic stimuli. Previously, we showed that, compared to dermal fibroblasts, gingival fibroblasts are less responsive to the potent pro-fibrotic cytokine TGFβ, due to a reduced production of endothelin-1 (ET-1). In this report, we show that, compared to dermal fibroblasts, human gingival fibroblasts show reduced expression of pro-adhesive mRNAs and proteins including integrins α2 and α4 and focal adhesion kinase (FAK). Consistent with these observations, gingival fibroblasts are less able to adhere to and spread on both fibronectin and type I collagen. Moreover, the enhanced production of ET-1 mRNA and protein in dermal fibroblasts is reduced by the FAK/src inhibitor PP2. Given our previous observations suggesting that fibrotic fibroblasts display elevated adhesive properties, our data suggest that scarring potential may be based, at least in part, on differences in adhesive properties among fibroblasts resident in connective tissue. Controlling adhesive properties may be of benefit in controlling scarring in response to tissue injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Adhesion*
  • Cells, Cultured
  • Endothelin-1 / genetics
  • Endothelin-1 / metabolism
  • Enzyme-Linked Immunosorbent Assay
  • Extracellular Matrix / metabolism*
  • Fibroblasts / cytology
  • Focal Adhesion Protein-Tyrosine Kinases / genetics
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism
  • Gene Expression Profiling
  • Gingiva / cytology*
  • Humans
  • Integrin alpha2 / genetics
  • Integrin alpha2 / metabolism
  • Integrin alpha4 / genetics
  • Integrin alpha4 / metabolism
  • Phosphorylation
  • RNA, Messenger / genetics
  • Real-Time Polymerase Chain Reaction
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Endothelin-1
  • Integrin alpha2
  • RNA, Messenger
  • Integrin alpha4
  • Focal Adhesion Protein-Tyrosine Kinases
  • p38 Mitogen-Activated Protein Kinases