胰高血糖素样肽2和肠上皮胰岛素样生长因子1受体在调节微绒毛长度中的作用。,Scientific Reports

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胰高血糖素样肽2和肠上皮胰岛素样生长因子1受体在调节微绒毛长度中的作用。
Scientific Reports ( IF 3.8 ) Pub Date : 2019-09-10 , DOI: 10.1038/s41598-019-49510-5
Melanie A Markovic ₁ , Patricia L Brubaker _{1,

2}

Affiliation

微绒毛是肠上皮细胞顶端的微小突起，有助于营养的吸收和吸收。它们的主要特征之一是长度均匀，但是人们对此却知之甚少。胰高血糖素样肽2（GLP-2）已显示可增加微绒毛长度，但需要其下游介质，肠上皮胰岛素样生长因子-1受体（IE-IGF-1R）和微绒毛蛋白由GLP-2采取的行动，至今未知。使用经长效人类（h）（GLY2）GLP-2或载体处理11d的IE-IGF-1R敲除（KO）小鼠，发现h（GLY2）GLP-2诱导的微绒毛增加长度需要IE-IGF-1R。此外，仅IE-IGF-1R KO导致微绒毛长度显着减少。刷状缘膜蛋白质组以及整个空肠黏膜的检查表明，h（GLY2）GLP-2处理以IE-IGF-1R依赖的方式增加了villin。在两种基础条件下以及h（GLY2）GLP-2处理IE-IGF-1R KO小鼠时，villin，IRTKS-1，harmonin，β-actin和myosin-1a的变化均不能解释微绒毛长度的减少，位于KO动物的刷状缘或空肠黏膜中。总的来说，这些研究为微绒毛中的IE-IGF-1R定义了新的作用，既在GLP-2诱导的信号级联反应中，也在内源性地起作用。Myosin-1a不能解释KO动物刷缘或空肠黏膜中微绒毛长度的减少。总的来说，这些研究为微绒毛中的IE-IGF-1R定义了新的作用，既在GLP-2诱导的信号级联反应中，也在内源性地起作用。Myosin-1a不能解释KO动物刷缘或空肠黏膜中微绒毛长度的减少。总的来说，这些研究为微绒毛中的IE-IGF-1R定义了新的作用，既在GLP-2诱导的信号级联反应中，也在内源性地起作用。

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The roles of glucagon-like peptide-2 and the intestinal epithelial insulin-like growth factor-1 receptor in regulating microvillus length.

Microvilli are tiny projections on the apical end of enterocytes, aiding in the digestion and absorption of nutrients. One of their key features is uniform length, but how this is regulated is poorly understood. Glucagon-like peptide-2 (GLP-2) has been shown to increase microvillus length but, the requirement of its downstream mediator, the intestinal epithelial insulin-like growth factor-1 receptor (IE-IGF-1R), and the microvillus proteins acted upon by GLP-2, remain unknown. Using IE-IGF-1R knockout (KO) mice, treated with either long-acting human (h) (GLY2)GLP-2 or vehicle for 11d, it was found that the h(GLY2)GLP-2-induced increase in microvillus length required the IE-IGF-1R. Furthermore, IE-IGF-1R KO alone resulted in a significant decrease in microvillus length. Examination of the brush border membrane proteome as well as of whole jejunal mucosa demonstrated that villin was increased with h(GLY2)GLP-2 treatment in an IE-IGF-1R-dependent manner. Under both basal conditions and with h(GLY2)GLP-2 treatment of the IE-IGF-1R KO mice, changes in villin, IRTKS-1, harmonin, β-actin, and myosin-1a did not explain the decrease in microvillus length, in either the brush border or jejunal mucosa of KO animals. Collectively, these studies define a new role for the IE-IGF-1R within the microvillus, in both the signaling cascade induced by GLP-2, as well as endogenously.

更新日期：2019-09-10

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