Angiotensin II induces monocyte chemoattractant protein‑1 expression by increasing reactive oxygen species‑mediated activation of the nuclear factor‑κB signaling pathway in osteoblasts.

Abstract

The present study investigated the effect of angiotensin II (AngII) on monocyte chemoattractant protein‑1 (MCP‑1) expression and the underlying mechanism in osteoblasts. MCP‑1 expression levels were analyzed by ELISA and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). AngII type 1 receptor (AT1R) expression levels was examined by RT‑qPCR, western blotting and immunostaining. In addition, the nuclear factor (NF)‑κB signaling pathway was investigated via western blot analysis. Reactive oxygen species (ROS) were also detected by flow cytometry and fluorescent microscopy. The results of the present study ndicated that AngII upregulated MCP‑1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N‑acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)‑κB, but not by the AngII type 2 receptor antagonist, PD123319. Furthermore, AngII increased the generation of ROS and activated the NF‑κB signaling pathway. These effects of AngII were blocked by olmesartan, NAC and PDTC, but not by PD1123319 in osteoblasts. In conclusion, these data indicated that AngII enhanced ROS production and activated NF‑κB signaling via AT1R, thus upregulating MCP‑1 expression in osteoblasts.