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首页> 外文期刊>Journal of Cellular Physiology >FGFR3 contributes to intestinal crypt cell growth arrest.
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FGFR3 contributes to intestinal crypt cell growth arrest.

机译：FGFR3有助于肠道隐窝细胞生长逮捕。

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摘要

Fibroblast growth factors (FGFs) are important regulators of the dynamic development and turnover of tissues. Among FGF receptors, FGFR3 expression is confined in the intestinal crypts. We examined FGFR3-deficient mice and saw increased intestinal crypt depth but no change in villae length or in the distribution of differentiated intestinal cells, suggesting that the impact of lack of FGFR3 was limited to the progenitor cell compartment. Accordingly, enhancement of intestinal crypt proliferation was observed in FGFR3 mutant mice and interestingly, upon anti-FGFR3 antibody administration in wild type mice. Moreover, injection of FGF18, a ligand of FGFR3, in wild type mice resulted in decreased cell proliferation within the intestinal crypts. In addition, we found that ERK level of activation was increased in FGFR3-deficient intestinal epithelium. In vitro studies showed that ERK, AKT and activation was regulated by FGFs and that ERK level of activation was inversely correlated to FGFR3 level of expression in the intestinal crypt cells. Furthermore, effects of FGF18 on ERK and AKT activation paralleled FGFR3 effects on these intracellular targets. Our data indicate that FGF18 and FGFR3 are involved, possibly as partners, in the control of intestinal precursor cell proliferation.
机译：纤维母细胞生长因子(fgf)是很重要的监管机构的动态发展营业额的组织。表达式是局限于肠道隐窝。我们检查了FGFR3-deficient老鼠,看到增加肠隐窝深度但没有变化villae长度或分布肠道细胞分化,说明缺乏FGFR3的影响是有限的祖细胞室。增强肠道隐窝的扩散观察到FGFR3突变小鼠和有趣的是,在anti-FGFR3抗体管理野生类型老鼠。FGFR3的野生型小鼠导致下降在肠隐窝细胞增殖。此外,我们发现ERK的水平激活是FGFR3-deficient增加肠道上皮细胞。受,一种蛋白激酶ERK和激活fgf ERK激活水平FGFR3指数呈现负相关的表达水平在肠道隐窝细胞。FGF18对ERK和AKT激活的影响对这些细胞内平行FGFR3的影响目标。可能,作为合作伙伴,在吗控制肠道细胞前体扩散。

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