|Title||Expression of integrin β1 by fibroblasts is required for tissue repair in vivo|
|Authors||Liu, S., Shi-Wen, X., Blumbach, K., Eastwood, M., Denton, C.P., Eckes, B., Krieg, T., Abraham, D.J. and Leask, A.|
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 β1 exhibit delayed cutaneous wound closure and less granulation tissue formation, including reduced production of new ECM and reduced expression of α-smooth muscle actin (α-SMA). Integrin-β1-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 α-SMA stress fiber formation. Loss of integrin β1 in adult fibroblasts reduced their ability to adhere to, to spread on and to contract ECM. Within stressed collagen matrices, integrin-β1-deficient fibroblasts showed reduced activation of latent TGFβ. Addition of active TGFβ alleviated the phenotype of integrin-β1-deficient mice. Thus integrin β1 is essential for normal wound healing, where it acts, at least in part, through a TGFβ-dependent mechanism in vivo.
|Journal||Journal of Cell Science|
|Journal citation||123 (21), pp. 3674-3682|
|Publisher||The Company of Biologists Ltd.|
|Digital Object Identifier (DOI)||https://doi.org/10.1242/jcs.070672|