| First Author | Frank S | Year | 2000 |
| Journal | J Clin Invest | Volume | 106 |
| Issue | 4 | Pages | 501-9 |
| PubMed ID | 10953025 | Mgi Jnum | J:112351 |
| Mgi Id | MGI:3656153 | Doi | 10.1172/JCI9148 |
| Citation | Frank S, et al. (2000) Leptin enhances wound re-epithelialization and constitutes a direct function of leptin in skin repair. J Clin Invest 106(4):501-9 |
| abstractText | Wound-healing disorders are a therapeutic problem of extensive clinical importance. Leptin-deficient ob/ob mice are characterized by a severely delayed wound healing that has been explained by the mild diabetic phenotype of these animals. Here we demonstrate that systemically and topically supplemented leptin improved re-epithelialization of wounds in ob/ob mice. Leptin completely reversed the atrophied morphology of the migrating epithelial tongue observed at the wound margins of leptin-deficient animals into a well-organized hyperproliferative epithelium. Moreover, topically supplemented leptin accelerated normal wound-healing conditions in wild-type mice. As assessed by immunohistochemistry, proliferating keratinocytes located at the wound margins specifically expressed the leptin-receptor subtype ObRb during repair. Additionally, leptin mediated a mitogenic stimulus to the human keratinocyte cell line HaCaT and human primary keratinocytes in vitro. Therefore, leptin might represent an effective novel therapeutic factor to improve impaired wound-healing conditions. |
