Fibroblast-specific focal adhesion kinase links mechanical force to fibrosis via chemokine-mediated inflammatory pathways

ABSTRACT: Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force t

ORGANISM(S): Mus musculus

SUBMITTER: Michael Januszyk 

PROVIDER: E-GEOD-26390 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress