mascRNA promotes macrophage apoptosis, inhibits osteoclast differentiation and attenuates disease progression in a murine model of arthritis.

Abstract

Macrophages play a crucial role in the pathogenesis of rheumatoid arthritis (RA) and have been considered as a therapeutic target of this disease. Here we show that mascRNA, a tRNA-like cytoplasmic small noncoding RNA, promoted RIPK1-dependent apoptosis (RDA) in RAW267.4 macrophages in response to the TAK1 inhibitor 5Z-7-oxozeaenol (5Z-7) alone as well as in combination with TNF. Moreover, mascRNA suppressed RANKL-induced expression of osteoclast marker genes and attenuated RANKL signaling. Using a murine model of collagen-induced arthritis (CIA), we demonstrated that mascRNA, administered either alone or in combination with 5Z-7, alleviated joint inflammation in CIA mice. Thus, mascRNA might be a promising agent for the treatment of RA.