Laboratory of Physiology, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka, 422-8526, Japan.
Department of Histology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto, 860-8556, Japan.
Sci Rep. 2020 Jun 25;10(1):10374. doi: 10.1038/s41598-020-67319-5.
Angulin-2/ILDR1 is a member of the angulin protein family, which is exclusively expressed at tricellular tight junctions in epithelia. Tricellular tight junctions are found where three cells meet and where three bicellular tight junction strands converge. Tricellular tight junctions are thought to be important for paracellular permeability of ions and water in epithelial tissues. It was recently reported that angulin-2/ILDR1 knockout mice have water transport abnormalities in the kidney. Since angulin-2/ILDR1 is the main tricellular tight junction protein in the large intestine, the goal of this research was to examine the effect of angulin-2/ILDR1 knockout on large intestinal paracellular water transport. We found that Ildr1 knockout mice showed no detectable phenotype other than deafness. In addition, paracellular transport as assessed by Ussing chamber was unchanged in Ildr1 knockout mice. However, we found that in the colon and the kidney of Ildr1 knockout mice, another tricellular tight junction protein, angulin-1/LSR, changes its expression pattern. We propose that with this replacement in tissue localization, angulin-1/LSR compensates for the loss of angulin-2/ILDR1 and maintains the barrier and function of the epithelia in the large intestine as well as the kidney.
Angulin-2/ILDR1 是 Angulin 蛋白家族的成员,仅在上皮细胞的三细胞紧密连接处表达。三细胞紧密连接处位于三个细胞相遇且两条双细胞紧密连接链汇聚的地方。三细胞紧密连接处被认为对于上皮组织中离子和水的旁细胞通透性很重要。最近有报道称,Angulin-2/ILDR1 敲除小鼠的肾脏存在水转运异常。由于 Angulin-2/ILDR1 是大肠中主要的三细胞紧密连接蛋白,因此本研究的目的是研究 Angulin-2/ILDR1 敲除对大肠旁细胞水转运的影响。我们发现,除了耳聋之外,Ildr1 敲除小鼠没有表现出可检测到的表型。此外,通过 Ussing 室评估的旁细胞转运在 Ildr1 敲除小鼠中没有改变。然而,我们发现,在 Ildr1 敲除小鼠的结肠和肾脏中,另一种三细胞紧密连接蛋白 Angulin-1/LSR 改变了其表达模式。我们提出,随着组织定位的这种替代,Angulin-1/LSR 补偿了 Angulin-2/ILDR1 的缺失,并维持了大肠和肾脏上皮的屏障和功能。