| First Author | Schulz JN | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 5 | Pages | 1435-1444 |
| PubMed ID | 25634355 | Mgi Jnum | J:220715 |
| Mgi Id | MGI:5635970 | Doi | 10.1038/jid.2015.24 |
| Citation | Schulz JN, et al. (2015) Reduced Granulation Tissue and Wound Strength in the Absence of alpha11beta1 Integrin. J Invest Dermatol 135(5):1435-44 |
| abstractText | Previous wound healing studies have failed to define a role for either alpha1beta1 or alpha2beta1 integrin in fibroblast-mediated wound contraction, suggesting the involvement of another collagen receptor in this process. Our previous work demonstrated that the integrin subunit alpha11 is highly induced during wound healing both at the mRNA and protein level, prompting us to investigate and dissect the role of the integrin alpha11beta1 during this process. Therefore, we used mice with a global ablation of either alpha2 or alpha11 or both integrin subunits and investigated the repair of excisional wounds. Analyses of wounds demonstrated that alpha11beta1 deficiency results in reduced granulation tissue formation and impaired wound contraction, independently of the presence of alpha2beta1. Our combined in vivo and in vitro data further demonstrate that dermal fibroblasts lacking alpha11beta1 are unable to efficiently convert to myofibroblasts, resulting in scar tissue with compromised tensile strength. Moreover, we suggest that the reduced stability of the scar is a consequence of poor collagen remodeling in alpha11(-/-) wounds associated with defective transforming growth factor-beta-dependent JNK signaling. |
