Leptin enhances wound re-epithelialization and constitutes a direct function of leptin in skin repair
Leptin enhances wound re-epithelialization and constitutes a direct function of leptin in skin repair
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DOI：
10.1172/jci9148
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发表时间：
2000-08-01
影响因子：
15.9
通讯作者：
Pfeilschifter, J
中科院分区：
文献类型：
--
作者：
Frank, S;Stallmeyer, B;Pfeilschifter, J
创伤愈合障碍是具有广泛临床重要性的治疗问题。瘦素缺乏的ob/ob小鼠的特征在于严重延迟的丘愈合，这已经被解释为这些动物的轻度糖尿病表型。在这里，我们证明了全身和局部补充瘦素改善了ob/ob小鼠伤口的上皮再生。瘦素完全逆转的萎缩形态的迁移上皮舌观察到的伤口边缘瘦素缺乏的动物成一个组织良好的过度增殖上皮。此外，局部补充瘦素加速野生型小鼠的正常伤口愈合条件。通过免疫组织化学评估，位于伤口边缘的增殖角质形成细胞在修复过程中特异性表达瘦素受体亚型ObRb。此外，瘦素介导的有丝分裂刺激的人角质形成细胞系HaCaT和人原代角质形成细胞在体外。因此，瘦素可能是一种有效的新的治疗因子，以改善受损的伤口愈合条件。
Wound-healing disorders are a therapeutic problem of extensive clinical importance. Leptin-deficient ob/ob mice are characterized by a severely delayed mound 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.