Abstract:
:Wound healing crucially relies on the mechanical activity of fibroblasts responding to TGFβ1 and to forces transmitted across focal adhesions. Integrin-linked kinase (ILK) is a central adapter recruited to integrin β1 tails in focal adhesions mediating the communication between cells and extracellular matrix. Here, we show that fibroblast-restricted inactivation of ILK in mice leads to impaired healing due to a severe reduction in the number of myofibroblasts, whereas inflammatory infiltrate and vascularization of the granulation tissue are unaffected. Primary ILK-deficient fibroblasts exhibit severely reduced levels of extracellular TGFβ1, α-smooth muscle actin (αSMA) production and myofibroblast conversion, which are rescued by exogenous TGFβ1. They are further characterized by elevated RhoA and low Rac1 activities, resulting in abnormal shape and reduced directional migration. Interference with RhoA-ROCK signaling largely restores morphology, migration and TGFβ1 levels. We conclude that, in fibroblasts, ILK is crucial for limiting RhoA activity, thus promoting TGFβ1 production, which is essential for dermal repair following injury.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Blumbach K,Zweers MC,Brunner G,Peters AS,Schmitz M,Schulz JN,Schild A,Denton CP,Sakai T,Fässler R,Krieg T,Eckes Bdoi
10.1242/jcs.063024subject
Has Abstractpub_date
2010-11-15 00:00:00pages
3872-83issue
Pt 22eissn
0021-9533issn
1477-9137pii
jcs.063024journal_volume
123pub_type
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