Interdisciplinary Program in Cancer Biology, College of Medicine, Seoul National University, Seoul 03080, Korea.
Korea Mouse Phenotyping Center, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Int J Mol Sci. 2020 Jan 17;21(2):614. doi: 10.3390/ijms21020614.
Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell-surface adhesion molecule that regulates cell migration and attachment. This study demonstrates the increase in Ninj1 protein expression during development of intestinal inflammation. Ninj1-deficient mice exhibited significantly attenuated bodyweight loss, shortening of colon length, intestinal inflammation, and lesser pathological lesions than wild-type mice. Although more severe inflammation and serious lesions are observed in wild-type mice than Ninj1-deficient mice, there were no changes in the numbers of infiltrating macrophages in the inflamed tissues obtained from WT and Ninj1-deficient mice. Ninj1 expression results in activation of macrophages, and these activated macrophages secrete more cytokines and chemokines than Ninj1-deficient macrophages. Moreover, mice with conditional deletion of Ninj1 in myeloid cells (Ninj1; Lyz-Cre+) alleviated experimental colitis compared with wild-type mice. In summary, we propose that the Ninj1 in myeloid cells play a pivotal function in intestinal inflammatory conditions.
神经损伤诱导蛋白 1（Ninjurin1，Ninj1）是一种细胞表面黏附分子，可调节细胞迁移和黏附。本研究表明，Ninj1 蛋白表达在肠道炎症发生过程中增加。Ninj1 缺陷型小鼠的体重减轻、结肠缩短、肠道炎症以及病理损伤明显低于野生型小鼠。尽管野生型小鼠的炎症比 Ninj1 缺陷型小鼠更严重，病变更严重，但在来自 WT 和 Ninj1 缺陷型小鼠的炎性组织中浸润的巨噬细胞数量没有变化。Ninj1 表达导致巨噬细胞活化，这些活化的巨噬细胞分泌的细胞因子和趋化因子比 Ninj1 缺陷型巨噬细胞多。此外，髓样细胞中 Ninj1 条件性缺失（Ninj1；Lyz-Cre+）的小鼠与野生型小鼠相比，实验性结肠炎得到缓解。总之，我们提出髓样细胞中的 Ninj1 在肠道炎症状态下发挥关键作用。
