Department of Microbiology, Nihon University School of Dentistry, Tokyo, Japan.
Connect Tissue Res. 2013;54(2):147-52. doi: 10.3109/03008207.2012.761978.
Visceral adipose tissue-derived serine protease inhibitor (vaspin), an adipokine that was recently identified in a rat model of type 2 diabetes, has been suggested to have an insulin-sensitizing effect. In this study, we investigated whether vaspin inhibits receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis using two types of osteoclast precursors: RAW264.7 cells and bone marrow cells (BMCs). Vaspin inhibited RANKL-induced osteoclastogenesis in RAW264.7 cells and BMCs. Interestingly, vaspin also inhibited the RANKL-induced expression of nuclear factor of activated T cells c1 (NFATc1) in RAW264.7 cells and BMCs. Furthermore, it inhibited the RANKL-induced upregulation of matrix metalloproteinase-9 and cathepsin K in RAW264.7 cells. Thus, we suggest that vaspin downregulates osteoclastogenesis in part by inhibiting expression of the transcription factor NFATc1.
内脏脂肪组织来源的丝氨酸蛋白酶抑制剂（vaspin）是一种在 2 型糖尿病大鼠模型中发现的脂肪因子，它被认为具有胰岛素增敏作用。在这项研究中，我们使用两种破骨细胞前体（RAW264.7 细胞和骨髓细胞（BMCs））研究了 vaspin 是否抑制核因子-κB 受体激活剂配体（RANKL）诱导的破骨细胞发生。vaspin 抑制了 RAW264.7 细胞和 BMCs 中 RANKL 诱导的破骨细胞发生。有趣的是，vaspin 还抑制了 RAW264.7 细胞和 BMCs 中核因子活化 T 细胞 c1（NFATc1）的 RANKL 诱导表达。此外，它抑制了 RAW264.7 细胞中基质金属蛋白酶-9 和组织蛋白酶 K 的 RANKL 诱导上调。因此，我们认为 vaspin 通过抑制转录因子 NFATc1 的表达部分地下调破骨细胞发生。
