Ontogeny of EGF receptors in the human gut

Ontogeny of EGF receptors in the human gut
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DOI:
10.2741/chailler
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发表时间:
1999-01-15
期刊:
Frontiers in Bioscience
影响因子:
--
通讯作者:
Menard, Daniel
Menard, Daniel
中科院分区:
其他
文献类型:
--
作者:
Chailler, Pierre;Menard, Daniel

文献摘要

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表皮生长因子及其相关物质通过与其基底外侧表面的高亲和力受体(EGF-R)结合来介导其对上皮细胞的影响,推测该生长因子系统在肠道形态发生和维持中起重要作用。本文重点分析了EGF-R在人胎儿肠段的表达和生化特征,并对EGF-R配体的生物学作用进行了探讨。它们似乎主要参与上皮细胞增殖的局部调节,其中EGF-R含量丰富。另一方面,EGF-R配体通过增加肠道乳糖酶活性和降低结肠刷状缘水解酶的活性来发挥一些早熟作用,同时下调末端分化的片段特异性标志物的表达,如肠道中的蔗糖酶、海藻糖酶和糖淀粉酶以及胃中的主细胞脂肪酶。这种作用与所有上皮细胞表面受体的鉴定是一致的,说明了EGF对分化的肠上皮细胞的调节作用。与动物模型的比较说明了受体的相似生化特性,并强调了人类肠道发育特有的生理方面。还讨论了配体异质性的相关性,并初步将其与不同的递送途径或生理反应联系起来。
Epidermal growth factor and related substances mediate their effects on epithelial cells through binding to high-affinity receptors (EGF-R) at their basolateral surface and it is hypothesized that this growth factor system play a major role in gut morphogenesis and maintenance. The current review emphasizes on analyzing the expression and the biochemical characteristics of EGF-R in human fetal gut segments and correlating the biological actions of EGF-R ligands. They appear to be primarily involved in the local regulation of epithelial cell proliferation in which EGF-R are abundant. Alternatively, EGF-R ligands exert some precocious maturative effects by increasing intestinal lactase activity and decreasing brush border hydrolases in colon while they down modulate the expression of segment-specific markers of terminal differentiation such as sucrase, trehalase and glucoamylase in the intestine and chief cell lipase in the stomach. Such effects are consistent with the identification of receptors at the surface of all epithelial cell types, illustrating the modulatory role of EGF on differentiated gut epithelial cells. Comparison with animal models illustrates similar biochemical properties of receptors and underlines physiological aspects specific to human gut development. The relevance for ligand heterogeneity is also discussed and tentatively associated with different delivery pathways or physiological responses.