| First Author | Neurohr C | Year | 2006 |
| Journal | Am J Respir Cell Mol Biol | Volume | 35 |
| Issue | 2 | Pages | 252-9 |
| PubMed ID | 16574941 | Mgi Jnum | J:123672 |
| Mgi Id | MGI:3718973 | Doi | 10.1165/rcmb.2006-0013OC |
| Citation | Neurohr C, et al. (2006) Activation of transforming growth factor-beta by the integrin alphavbeta8 delays epithelial wound closure. Am J Respir Cell Mol Biol 35(2):252-9 |
| abstractText | Transforming growth factor (TGF)-beta family members regulate multiple aspects of wound repair through effects on cell proliferation, matrix production, and tissue inflammation, but the effects of TGF-beta on wound closure itself have been controversial. We found that blocking antibodies to TGF-beta enhanced the degree of closure of scratch wounds in primary airway epithelial monolayers, while addition of exogenous TGF-beta1 inhibited the degree of closure, suggesting that endogenous activation of TGF-beta normally serves as a brake on the degree of wound closure. Although these cells secreted large amounts of TGF-beta2 and small amounts of TGF-beta1, blockade of TGF-beta1 enhanced the degree of wound closure, whereas blockade of TGF-beta2 had no effect. TGF-beta1 (but not TGF-beta2) can be activated by two members of the integrin family, alphavbeta6 and alphavbeta8, which are both expressed on airway epithelial cells. Wounding induced activation of TGF-beta through effects of both integrins, but antibodies against alphavbeta8 enhanced the degree of wound closure, whereas antibodies against alphavbeta6 did not. |
