Tomiyama Shiori, Nakamachi Tomoya, Uchiyama Minoru, Matsuda Kouhei, Konno Norifumi
Department of Biological Science, Graduate School of Science and Engineering, University of Toyama, 3190 Gofuku, Toyama 930-8555, Japan.
Department of Biological Science, Graduate School of Science and Engineering, University of Toyama, 3190 Gofuku, Toyama 930-8555, Japan.
Gen Comp Endocrinol. 2015 May 15;216:54-63. doi: 10.1016/j.ygcen.2015.04.009. Epub 2015 Apr 20.
Urotensin II (UII) exhibits diverse physiological actions including vasoconstriction, locomotor activity, osmoregulation, and immune response via the UII receptor (UTR) in mammals. However, in amphibians the function of the UII-UTR system remains unknown. In the present study, we investigated the potential immune function of UII using leukocytes isolated from the African clawed frog, Xenopus laevis. Stimulation of male frogs with lipopolysaccharide increased mRNA expression of UII and UTR in leukocytes, suggesting that inflammatory stimuli induce activation of the UII-UTR system. Migration assays showed that both UII and UII-related peptide enhanced migration of leukocytes in a dose-dependent manner, and that UII effect was inhibited by the UTR antagonist urantide. Inhibition of Rho kinase with Y-27632 abolished UII-induced migration, suggesting that it depends on the activation of RhoA/Rho kinase. Treatment of isolated leukocytes with UII increased the expression of several cytokine genes including tumor necrosis factor-α, interleukin-1β, and macrophage migration inhibitory factor, and the effects were abolished by urantide. These results suggest that in amphibian leukocytes the UII-UTR system is involved in the activation of leukocyte migration and cytokine gene expression in response to inflammatory stimuli.
尾加压素II（UII）在哺乳动物中通过尾加压素II受体（UTR）表现出多种生理作用，包括血管收缩、运动活性、渗透调节和免疫反应。然而，在两栖动物中，UII-UTR系统的功能仍然未知。在本研究中，我们使用从非洲爪蟾（非洲爪蟾）分离的白细胞研究了UII的潜在免疫功能。用脂多糖刺激雄性爪蟾会增加白细胞中UII和UTR的mRNA表达，这表明炎症刺激会诱导UII-UTR系统的激活。迁移试验表明，UII和UII相关肽均以剂量依赖性方式增强白细胞的迁移，并且UII的作用被UTR拮抗剂尿紧张素抑制。用Y-27632抑制Rho激酶可消除UII诱导的迁移，这表明它依赖于RhoA/Rho激酶的激活。用UII处理分离的白细胞会增加包括肿瘤坏死因子-α、白细胞介素-1β和巨噬细胞迁移抑制因子在内的几种细胞因子基因的表达，并且这些作用被尿紧张素消除。这些结果表明，在两栖动物白细胞中，UII-UTR系统参与了炎症刺激下白细胞迁移和细胞因子基因表达的激活。
