Role of MAPK signal pathways in differentiation process of M2 macrophages induced by high-ambient glucose and TGF-β1. (3rd September 2015)

• Record Type: Journal Article
• Authors: Su, Ning; Li, Yafang; Wang, Jie; Fan, Jinjin; Li, Xiaoyan; Peng, Wenxing; Yu, Xueqing; Zhou, Tian-Biao; Jiang, Zongpei
• Is Part Of: Journal of receptor and signal transduction research. Volume 35:Number 5(2015)
• Page Start: 396
• Page End: 401
• Publication Date: 2015-09-03
• Subjects: ERK -- high-ambient glucose -- macrophage -- RAW264.7 cells -- TGF-β1; Cell receptors -- Periodicals; Cellular signal transduction -- Periodicals; 571.6
• DOI: 10.3109/10799893.2014.960933
• Languages: English
• ISSNs: 1079-9893

Abstract

Abstract: Macrophage can be alternatively activated by TGF-β1, whether high-ambient glucose can enhance the sensitivity of TGF-β1 and the intracellular mechanisms involved in this process are not fully understood. We examined whether the mitogen-activated protein kinase is involved in the activation of macrophage induced by TGF-β1 and high-ambient glucose. The expression of arginase-1, CD206 and TGF-β1 was accessed by Western blot and immunofluorescence in RAW 264.7 cells stimulated with TGF-β1 and high-ambient glucose. The activation of MAPK pathways in the process was investigated by Western blot. The role of MAPK was assessed using biochemical inhibitors. The protein of arginase-1, CD206 and TGF-β1 was significantly overexpressed in RAW264.7 cells stimulated by TGF-β1 and high-ambient glucose. ERK and JNK phosphorylation occurred in 30 min and p38MAPK phosphorylation occurred in 30 min and 24 h after the stimulation. And the expression of arginase-1 and TGF-β1 was partially blocked by the pretreated ERK biochemical inhibitor (U0126) instead of the JNK inhibitor (SP600125) and p38MAPK inhibitor (SB203580). In conclusion, high-ambient glucose can enhance the sensitivity of TGF-β1 in RAW264.7 cells, which resulted in overexpression of TGF-β1 and arginase-1 in macrophages. ERK plays a role in this process.