EGF和EGFR: IBD中调节炎症和粘膜愈合治疗的有希望的靶点

Evanna Huynh, Julang Li
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引用次数: 4

摘要

克罗恩病是炎症性肠病(IBD)的主要类型。这种疾病可能与肠黏膜无法保护自身免受肠道损伤或肠损伤后上皮修复缺陷有关。粘膜愈合依赖于肠上皮细胞(IEC)的恢复、增殖和分化等协调事件。根据我们之前的研究,表皮生长因子(EGF)可以提高早期断奶猪的生长性能,我们最近研究了表皮生长因子在促进肠道发育和减少炎症方面的潜在体内机制。通过基因表达、酶活性和组织形态学分析,研究了egf介导的保护作用的机制。进一步的证据表明,EGFR和GLP2R与下游信号通路有关,从而增强KGF和Muc2等保护性腔因子的表达。EGFR信号的多方面网络效应使这种受体及其原型配体EGF成为粘膜愈合治疗的有希望的靶点。
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EGF and EGFR: Promising targets for modulating inflammation and mucosal healing therapy in IBD
Crohn’s disease is a major type of inflammatory bowel disease (IBD). This disease may be associated with an inability of the intestinal mucosa to protect itself from luminal challenges or defective epithelial repair following intestinal injury. Mucosal healing relies on coordinated events consisting of intestinal epithelial cell (IEC) restitution, proliferation and differentiation. From our previous work leading to epidermal growth factor (EGF) enhancing growth performance in early-weaned pigs, we recently addressed potential in vivo mechanisms of EGF in enhancing intestine development and reducing inflammation.  The mechanisms underlying the EGF-mediated protective effects were investigated by gene expression, enzyme activity, and histomorphology analyses. Further evidence linking EGFR and GLP2R to downstream signaling pathways to enhance the expression of protective luminal factors such as KGF and Muc2 was demonstrated. The multi-faceted network effect of EGFR signaling allows this receptor and its prototypical ligand, EGF, to emerge as promising targets for mucosal healing therapy.
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