Loss of Integrin-Linked Kinase Leads to Dysplasia of the Colon in Mice
Loss of Integrin-Linked Kinase Leads to Dysplasia of the Colon in Mice
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DOI：
10.1142/s1793984421400067
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发表时间：
2021-07
期刊：
影响因子：
0.8
通讯作者：
Yujie Gao;Siyi Xie;Chushan Fang;Yunfu Sun;Xingqun Liang
中科院分区：
文献类型：
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作者：
Yujie Gao;Siyi Xie;Chushan Fang;Yunfu Sun;Xingqun Liang
结肠的正常发育对一生的健康至关重要。整合素连接激酶（ILK）是整合素信号通路的关键部分，连接细胞内和细胞外信号通路，并且在进化上是保守的。已显示ILK敲除可导致各种器官的异常形成。在我们的研究中，我们发现通过血小板衍生生长因子受体B（PDGFR[式：见正文]-Cre）缺失ILK导致神经嵴细胞（NCC）的异常迁移和胃肠道缩短，沿着结肠腔的扩张和肠神经纤维的发育不良。总之，ILK是正常结肠发育所必需的。
Normal development of the colon is essential for well-being during the life span. Integrin linked kinase (ILK), which is a key part of the integrin signaling pathway, connects intracellular and extracellular signaling pathways and is evolutionally conserved. It has been shown that ILK knockouts can lead to abnormal formation of various organs. In our study, we found that deletion of ILK by platelet-derived growth factor receptor B (PDGFR[Formula: see text]-Cre leads to the abnormal migration of neural crest cells (NCCs) and the shortening of the gastrointestinal tract, along with the expansion of the colon cavity and dysplasia of the intestinal nerve fibers. In conclusion, ILK is required for normal colon development.