Su Ning, Xiao Chaoxing, Wei Yi, Kou Qiuye, Jiang Zongpei
a Department of Nephrology , the Six Affiliated Hospital of Sun Yat-sen University , Guangzhou , China.
J Recept Signal Transduct Res. 2018 Feb;38(1):27-30. doi: 10.1080/10799893.2017.1407340. Epub 2017 Dec 4.
Macrophages can be alternatively activated by TGF-β1 and high-ambient glucose, in which the role of Smad2 and the crosstalk between ERK and Smad2 pathways are not fully understood. The activation of ERK and Smad2 pathways and the expression of arginase-1 were detected by Western blot. The role of Smad2 and the relationship between ERK and Smad2 pathways were investigated by using biochemical inhibitors. The protein of arginase-1 was significantly overexpressed in RAW264.7 cells stimulated by TGF-β1 and high-ambient glucose, which can be partially blocked by not only U0126 (ERK inhibitor) but also SB431542 (Smad2 inhibitor). Furthermore, simply inhibiting one pathway had no effect on the other pathway. In conclusion, both ERK and Smad2 signal pathways are involved in the activation of macrophages induced by TGF-β1 and high-ambient glucose, while there is no crosstalk shown in the process.
巨噬细胞可被转化生长因子-β1(TGF-β1)和高环境葡萄糖选择性激活,其中Smad2的作用以及细胞外信号调节激酶(ERK)与Smad2信号通路之间的相互作用尚未完全明确。通过蛋白质免疫印迹法检测ERK和Smad2信号通路的激活情况以及精氨酸酶-1的表达。使用生化抑制剂研究Smad2的作用以及ERK与Smad2信号通路之间的关系。在TGF-β1和高环境葡萄糖刺激的RAW264.7细胞中,精氨酸酶-1蛋白显著过表达,这不仅可被U0126(ERK抑制剂)部分阻断,也可被SB431542(Smad2抑制剂)部分阻断。此外,单纯抑制一条信号通路对另一条信号通路没有影响。总之,ERK和Smad2信号通路均参与TGF-β1和高环境葡萄糖诱导的巨噬细胞激活过程,且在此过程中未显示出相互作用。