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首页> 外文期刊>Journal of cellular physiology. >DOCK4 stimulates MUC2 production through its effect on goblet cell differentiation
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DOCK4 stimulates MUC2 production through its effect on goblet cell differentiation

机译：通过其DOCK4刺激MUC2生产对杯状细胞分化的影响

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摘要

The intestinal mucosa is in continuous contact with milliard of microorganisms, thus intestinal epithelial barrier is a critical component in the arsenal of defense mechanisms required to prevent infection and inflammation. Mucin 2 (MUC2), which is produced by the goblet cells, forms the skeleton of the intestinal mucus and protects the intestinal tract from self-digestion and numerous microorganisms. Dedicator of cytokinesis 4 (DOCK4) is a member of the DOCK-B subfamily of the DOCK family of guanine nucleotide exchange factors. It is reported that DOCK4 plays a critical role in the repair of the barrier function of the intestinal epithelium after chemical damage. In this study, the role of DOCK4 in the goblet cell differentiation and MUC2 production is explored. Disordered intestinal epithelium and shortage of goblet cells were observed in DOCK4 gene knockout mice. Furthermore, DOCK4 deletion contributed to the low expression of MUC2 and the goblet cell differentiation/maturation factors including growth factor independent 1 (Gfi1) and SAM pointed domain epithelial-specific transcription factor (Spdef) in mouse ileums and colons. Overexpression of DOCK4 caused a marked increase in Gfi1, Spdef, and MUC2, while siRNA knockdown of endogenous DOCK4 significantly decreased Gfi1, Spdef, and MUC2 in HT-29 cells. In addition, MUC2, DOCK4, and the goblet cell differentiation/maturation factors mRNA levels were decreased in colorectal cancer samples compared with normal colons. A significant positive correlation was found between MUC2 and DOCK4. In conclusion, DOCK4 may serve as a critical regulator of goblet cell differentiation and MUC2 production in the intestine.
机译：肠道粘膜是在连续接触与成千上万的微生物,因此肠上皮屏障中是一个关键组件阿森纳的防御机制必须防止感染和炎症。是由杯状细胞,形成了吗骨架的肠道粘液和保护肠道self-digestion和众多微生物。(DOCK4)属于DOCK-B亚科码头的鸟嘌呤核苷酸交换的因素。关键作用的修复障碍后肠上皮细胞的功能化学损伤。杯状细胞分化和MUC2探讨了生产。上皮细胞和杯状细胞短缺观察到DOCK4基因敲除小鼠。此外,DOCK4删除了低MUC2的表达和杯状细胞分化成熟等因素生长因子独立1 (Gfi1)和山姆指出域epithelial-specific转录在鼠标回肠和冒号因子(Spdef)。过度的DOCK4显著增加引起的在Spdef Gfi1和MUC2, siRNA击倒内生Gfi1 DOCK4大大降低,Spdef和MUC2 HT-29细胞。MUC2 DOCK4,杯状细胞分化/成熟因子mRNA水平减少结直肠癌样品吗相比之下,普通的冒号。积极MUC2和之间的相关性被发现DOCK4。杯状细胞分化的关键调节器在小肠和MUC2生产。

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