MAP kinases in regulation of NOX activity stimulated through two types of formyl peptide receptors in murine bone marrow granulocytes

The functional activity of the phagocytes, as well as the development and resolution of the inflammation, is determined by formylpeptide receptors (FPRs) signaling. There is a growing data on the signaling pathways from two major types of formylpeptide receptors, FPR1 and FPR2, which could be activated by different sets of ligands to provide certain defense functions. Generation of reactive oxygen species (ROS) by the membrane enzyme NADPH oxidase is the most important among them. One of the most studied and significant mechanism for the regulation of activity of NADPH oxidase is phosphorylation by a variety of kinases, including MAP kinases. The question arose whether the role of MAPKs differ in the activation of NADPH oxidase through FPR1 and FPR2. We have studied Fpr1-and Fpr2-induced phosphorylation of p38, ERK, and JNK kinases and their role in the activation of the respiratory burst in isolated mice bone marrow granulocytes. Data has shown distinct patterns of MAP kinase activity for Fpr1 and Fpr2: JNK was involved in both Fpr1 and Fpr2 mediated activation of ROS production, while p38 MAPK and ERK were involved in Fpr1 induced ROS generation only.

Automated summary

Phagocytes' functional activity and inflammation's development and resolution are determined by formylpeptide receptors (FPRs) signaling. Research has shown that different types of formylpeptide receptors, FPR1 and FPR2, activate distinct patterns of MAP kinase activity, with JNK involved in both Fpr1 and Fpr2 mediated activation of ROS production, while p38 MAPK and ERK are only involved in Fpr1 induced ROS generation.