MiR-30a attenuates osteoclastogenesis via targeting DC-STAMP-c-Fos-NFATc1 signaling.

Osteoclast is a kind of unique cells which is responsible for bone matrix absorption. It was widely reported that microRNAs (miRNAs) could regulate several physiological processes, including osteoclastogenesis. In our study, microarray analysis showed that miR-30a was down-regulated during osteoclastogenesis after RANKL (receptor activator of nuclear factor κB ligand) stimulation. Osteoclasts and actin-ring formation as well as bone resorption were inhibited when miR-30a was overexpressed in osteoclast precursor cells. Meantime, when miR-30a was inhibited in osteoclast precursor cells, osteoclasts and actin-ring formation as well as bone resorption were promoted. Furthermore, we discovered that miR-30a overexpression inhibited the protein levels of DC-STAMP, c-Fos and NFATc1. However, when DC-STAMP was inhibited by using a DC-STAMP siRNA, we could not detect the inhibition effect of osteoclastogenesis and bone resorption induced by miR-30a. In conclusion, miR-30a attenuated osteoclastogenesis via suppression of DC-STAMP-c-Fos-NFATc1 signaling pathway. On these grounds, this study may reveal a new promising target for the treatment of osteoporosis and other osteopenic disorders.