EGFR enhances early healing after cutaneous incisional wounding
EGFR enhances early healing after cutaneous incisional wounding
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DOI：
10.1111/j.0022-202x.2004.23478.x
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发表时间：
2004-11-01
影响因子：
6.5
通讯作者：
Hansen, LA
中科院分区：
文献类型：
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作者：
Repertinger, SK;Campagnaro, E;Hansen, LA
表皮生长因子受体（EGFR）参与了伤口愈合的调节。为了直接评价内源性EGFR在皮肤切口伤口愈合中的作用，我们检查了损伤后EGFR缺失和野生型皮肤。在创伤后5天，表皮再生在所有EGFR野生型伤口中完成，但在EGFR无效伤口中仅为40%。EGFR缺失皮肤中的伤口闭合延迟伴有水肿增加、焦痂持续时间更长且更突出以及对合伤口边缘之间的距离增加。EGFR改变中性粒细胞和肥大细胞浸润，并增强血管生成。表皮生长因子受体增强上皮细胞的增殖在第一个3天受伤后，虽然增殖是更大的表皮生长因子受体无效伤口在5天。虽然与对照组相比，EGFR空角化细胞与标准培养基或培养基中补充转化生长因子-α培养的迁移减少，但加入伤口相关的运动原角化细胞生长因子消除了基因型之间的差异。表皮生长因子受体阴性皮肤中上皮细胞向伤口的迁移减少，表明表皮生长因子受体依赖性和非依赖性机制在伤口愈合过程中调节迁移。这些数据表明EGFR调节皮肤伤口愈合的多个方面，包括炎症、伤口收缩、增殖、迁移和血管生成。
The epidermal growth factor receptor (EGFR) has been implicated in the regulation of wound healing. In order to directly evaluate the role of endogenous EGFR in cutaneous incisional wound healing, we examined EGFR null- and wild-type skin after injury. By 5 d after wounding, re-epithelialization was complete in all EGFR wild-type wounds, but in only 40% of EGFR null wounds. Delayed wound closure in EGFR null skin was accompanied by an increase in edema, longer lasting and more prominent eschar, and increased distance between apposing wound edges. EGFR altered neutrophil and mast cell infiltration, and enhanced angiogenesis. EGFR enhanced epithelial proliferation during the first 3 d following injury, although proliferation was greater in EGFR null wounds at 5 d. Although migration was decreased in EGFR null keratinocytes cultured with standard medium or in medium supplemented with transforming growth factor-alpha when compared with controls, the addition of the wound-associated motogen keratinocyte growth factor eliminated the differences between genotypes. Epithelial migration into the wound was decreased in EGFR null skin, suggesting that both EGFR-dependent and -independent mechanisms regulate migration during wound healing. These data demonstrate that EGFR regulates multiple facets of cutaneous wound healing, including inflammation, wound contraction, proliferation, migration, and angiogenesis.