Caveolin-1 in extracellular matrix vesicles secreted from osteoblasts

Caveolin-1 in extracellular matrix vesicles secreted from osteoblasts
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DOI：
10.1016/j.bone.2007.02.030
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发表时间：
2007-07-01
期刊：
BONE
影响因子：
4.1
通讯作者：
Takeda, Eiji
Takeda, Eiji
中科院分区：
医学2区
文献类型：
--
作者：
Sawada, Naoki;Taketani, Yutaka;Takeda, Eiji

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小窝蛋白-1是小窝的必需和标志性蛋白，小窝是富含胆固醇和鞘脂的质膜的小内陷。尽管caveolin-1在成骨细胞、内皮细胞、成纤维细胞和肌肉细胞中的高水平表达已被证实，但caveolin-1在成骨细胞中的作用尚未阐明。在这里，我们表明，小窝蛋白-1是从成骨细胞分泌的基质囊泡的形式，细胞外囊泡从成骨细胞的质膜释放。在这项研究中，小窝和基质囊泡同样富含胆固醇和鞘磷脂的馏分分离矿化MC 3 T3-E1细胞。有趣的是，在MC 3 T3-E1细胞中，小窝蛋白-1富集在基质囊泡组分以及小窝膜组分中，并且随着分化的进行，基质囊泡组分中的小窝蛋白-1的量增加。在小鼠胫骨中也证实了小窝蛋白-1在基质囊泡中的定位。此外，过度表达caveolin-1可增强MC 3 T3-E1细胞的基质钙化，而敲低caveolin-1则可减弱这种钙化，这些结果表明，分泌的caveolin-1作为基质囊泡的一种成分，可能在成骨细胞钙化中起重要作用。(c)2007年爱思唯尔公司All rights reserved.
Caveolin-1 is an essential and signature protein of caveolae, which are small invaginations of the plasma membrane enriched in cholesterol and sphingolipids. Although high levels of expression of caveolin-1 have been demonstrated in osteoblasts as welt as endothelial cells, fibroblasts, and muscular cells, the role of caveolin-1 in osteoblasts has not been clarified. Here, we show that caveolin-1 is secreted from osteoblasts in the form of matrix vesicles; extracellular vesicles released from the plasma membrane of osteoblasts. In this study, caveolae and matrix vesicles were similarly enriched in cholesterol and sphingomyelin in fractions isolated from mineralizing MC3T3-E1 cells. Interestingly, in the MC3T3-E1 cells caveolin-1 was enriched in the matrix vesicle fraction as well as the caveolar membrane fraction, and the amount of caveolin-1 in the matrix vesicle fraction increased as differentiation progressed. Localization of caveolin-1 in matrix vesicles was also confirmed in murine tibia. Furthermore, overexpression of caveolin-1 enhanced matrix calcification in MC3T3-E1 cells, whereas knockdown of caveolin-1 diminished it. These results suggest that secreted caveolin-1 as a component of matrix vesicles may play an important role in osteoblast calcification. (c) 2007 Elsevier Inc. All rights reserved.