| First Author | Liu S | Year | 2010 |
| Journal | J Cell Sci | Volume | 123 |
| Issue | Pt 21 | Pages | 3674-82 |
| PubMed ID | 20940256 | Mgi Jnum | J:182925 |
| Mgi Id | MGI:5317088 | Doi | 10.1242/jcs.070672 |
| Citation | Liu S, et al. (2010) Expression of integrin beta1 by fibroblasts is required for tissue repair in vivo. J Cell Sci 123(Pt 21):3674-82 |
| abstractText | In tissue repair, fibroblasts migrate into the wound to produce and remodel extracellular matrix (ECM). Integrins are believed to be crucial for tissue repair, but their tissue-specific role in this process is poorly understood. Here, we show that mice containing a fibroblast-specific deletion of integrin beta1 exhibit delayed cutaneous wound closure and less granulation tissue formation, including reduced production of new ECM and reduced expression of alpha-smooth muscle actin (alpha-SMA). Integrin-beta1-deficient fibroblasts showed reduced expression of type I collagen and connective tissue growth factor, and failed to differentiate into myofibroblasts as a result of reduced alpha-SMA stress fiber formation. Loss of integrin beta1 in adult fibroblasts reduced their ability to adhere to, to spread on and to contract ECM. Within stressed collagen matrices, integrin-beta1-deficient fibroblasts showed reduced activation of latent TGFbeta. Addition of active TGFbeta alleviated the phenotype of integrin-beta1-deficient mice. Thus integrin beta1 is essential for normal wound healing, where it acts, at least in part, through a TGFbeta-dependent mechanism in vivo. |
