| First Author | Chmielowiec J | Year | 2007 |
| Journal | J Cell Biol | Volume | 177 |
| Issue | 1 | Pages | 151-62 |
| PubMed ID | 17403932 | Mgi Jnum | J:133551 |
| Mgi Id | MGI:3778834 | Doi | 10.1083/jcb.200701086 |
| Citation | Chmielowiec J, et al. (2007) c-Met is essential for wound healing in the skin. J Cell Biol 177(1):151-62 |
| abstractText | Wound healing of the skin is a crucial regenerative process in adult mammals. We examined wound healing in conditional mutant mice, in which the c-Met gene that encodes the receptor of hepatocyte growth factor/scatter factor was mutated in the epidermis by cre recombinase. c-Met-deficient keratinocytes were unable to contribute to the reepithelialization of skin wounds. In conditional c-Met mutant mice, wound closure was slightly attenuated, but occurred exclusively by a few (5%) keratinocytes that had escaped recombination. This demonstrates that the wound process selected and amplified residual cells that express a functional c-Met receptor. We also cultured primary keratinocytes from the skin of conditional c-Met mutant mice and examined them in scratch wound assays. Again, closure of scratch wounds occurred by the few remaining c-Met-positive cells. Our data show that c-Met signaling not only controls cell growth and migration during embryogenesis but is also essential for the generation of the hyperproliferative epithelium in skin wounds, and thus for a fundamental regenerative process in the adult. |
