Loss of Integrin-Linked Kinase Leads to Dysplasia of the Colon in Mice

IF 0.8 Q4 MATERIALS SCIENCE, BIOMATERIALS Nano Life Pub Date : 2021-07-23 DOI:10.1142/s1793984421400067
Yujie Gao, Siyi Xie, Chushan Fang, Yunfu Sun, Xingqun Liang
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Abstract

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.
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整合素连接激酶缺失导致小鼠结肠发育不良
结肠的正常发育对其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,在进化上是保守的。已经表明ILK敲除可导致各种器官的异常形成。在我们的研究中,我们发现血小板衍生生长因子受体B(PDGFR[公式:见正文]-Cre)缺失ILK会导致神经嵴细胞(NCCs)的异常迁移和胃肠道缩短,同时导致结肠腔扩张和肠神经纤维发育不良。总之,ILK是正常结肠发育所必需的。
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来源期刊
Nano Life
Nano Life MATERIALS SCIENCE, BIOMATERIALS-
CiteScore
0.70
自引率
12.50%
发文量
14
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