Osteoclast stimulatory transmembrane protein induces a phenotypic switch in macrophage polarization suppressing an M1 pro-inflammatory state

Abstract

Macrophages are the key cells in metabolic syndrome and are also a risk factor for metabolic disease. Macrophages have different functions and transcriptional profiles, but all are required for maintaining homeostasis. It is well known that macrophages play a key role in inflammation and early atherogenesis, and are present in two phenotypes: pro-inflammatory (M1) and anti-inflammatory (M2). Osteoclast stimulatory transmembrane protein (oc-stamp) is a multiple-pass transmembrane protein; however, its function remains unclear. In this study, we explored the role of oc-stamp in macrophages physiology. The results showed that oc-stamp was notably decreased under LPS and IFN-γ stimulation, while it was increased with IL-4 treatment. Furthermore, oc-stamp induced a phenotypic switch in macrophage polarization, suppressing the M1 pro-inflammatory state in the overexpression group, and promoting the M1 pro-inflammatory state in the knockdown group. Further study revealed that oc-stamp regulated macrophage polarization possibly via STAT6. Taken together, our results are the first to demonstrate that oc-stamp may play an important role in macrophage polarization and inhibit the M1 pro-inflammatory state.

Keywords: STAT6; inflammation; macrophage polarization; oc-stamp.