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. 2010 Jan 15;11(2):97–105. doi: 10.1038/embor.2009.276

Figure 2.

Figure 2

Integrin–TGF-β crosstalk mechanisms. (A) In fibrosis and sclerosis, TGF-β signalling induces fibroblast differentiation into contractile myofibroblasts. The myofibroblasts express and deposit collagen (1), express α1β1- and α2β1-integrins that mediate collagen remodelling and contraction (2), and express αv-integrins that activate latent TGF-β from the matrix (3). (B) During TGF-β-mediated EMT of alveolar epithelial cells, integrin α3β1 forms a complex with TGF-βRs and E-cadherin, facilitating β-catenin–Smad2 complex formation and nuclear translocation. (C) During malignant progression, TGF-β frequently represses the expression of laminin and/or laminin-binding integrins α3β1 and α6β4, and induces the expression of fibronectin and integrins α5β1 and αvβ6. αvβ6 mediates migration and invasion and generates new active TGF-β, stimulating other tumour cells as well as myofibroblast differentiation in the tumour stroma. β-cat, β-catenin; Col, collagen; E-cadh, E-cadherin; EMT, epithelial-to-mesenchymal transition; FN, fibronectin; LN332, laminin 332; TGF-β, transforming growth factor-β; TGF-βR, transforming growth factor-β receptor.