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The important role of miR-133a in the progress and development of postmenopausal osteoporosis has been reported,however,the underlying mechanism is not clear yet.In this study,qRT-PCR analysis was performed to assess miR-133 expression in serum isolated from postmenopausal osteoporosis patients (PMOP) and healthy controls.Bone mineral density (BMD) was measured at the lumbar spine by dual-energy X-ray absorptiometry (DXA).The results showed that miR-133a was significantly upregulated and negatively correlated with lumbar spine BMD in serum of postmenopausal osteoporotic women.The miR-133a mimic,miR-133a inhibitor,and the corresponding controls were transfected into RAW264.7 and THP-1 cells,respectively.TRAP-positive cells were counted and the protein expression of NFATcl,c-Fos and TRAP were detected by weste blot analysis.We found that MiR-133a was upregulated during osteoclastogenesis,and overexpression of miR-133a promoted RANKL-induced differentiation of RAW264.7 and THP-1 cells into osteoclasts,whereas miR-133a knockdown showed the reversed results.In in vivo experiment,rats were bilaterally ovariectomized (OVX) and injected with antagomiR-133a or antagoNC,and were sacrificed for collecting serum and lumbar spine for ELISA,micro-computed Tomography (CT) and bone histomorphology analysis,respectively.It was found that,in OVX rats,miR-133a knockdown altered the levels of osteoclastogenesis-related factors in serum and increased lumbar spine BMD and changed bone histomorphology.Collectively,miRNA-133a is involved in the regu lation of postmenopausal osteoporosis through promoting osteoclast differentiation.