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前列腺素E2对培养的胎儿长骨中巨噬细胞和破骨细胞的影响。

Effects of prostaglandin E2 on macrophages and osteoclasts in cultured fetal long bones.

作者信息

Rifkin B R, Baker R L, Coleman S J

出版信息

Cell Tissue Res. 1980;207(2):341-6. doi: 10.1007/BF00237817.

Abstract

Bone cultures exposed to prostaglandin E2 (PGE2) and revealed an increase in 45Ca release from bone to medium and an increase in osteoclast number compared to control bones. In addition, PGE2-treated osteoclasts contained a more extensive ruffled border region than control osteoclasts. These data suggest that PGE2 activates existing osteoclasts and causes proliferation and differentiation of osteoclast precursor cells. The existence of macrophages in resorbing fetal bone explants was documented. These macrophages contain numerous phagolysosomes and lipid vacuoles and are often located adjacent ot osteoclasts or closely apposed to calcified tissue surfaces. PGE2 caused an early increase in the number of macrophages. It is postulated that fetal bone macrophages are primarily engaged in phagocytosis and digestion of cellular debris, but also play a role in the process of bone resorption.

摘要

暴露于前列腺素E2(PGE2)的骨培养物显示,与对照骨相比,从骨到培养基的45Ca释放增加,破骨细胞数量增加。此外,经PGE2处理的破骨细胞比对照破骨细胞含有更广泛的褶皱边缘区域。这些数据表明,PGE2激活现有的破骨细胞,并导致破骨细胞前体细胞的增殖和分化。在正在吸收的胎儿骨外植体中记录到巨噬细胞的存在。这些巨噬细胞含有大量吞噬溶酶体和脂质空泡,并且通常位于破骨细胞附近或紧密贴附于钙化组织表面。PGE2导致巨噬细胞数量早期增加。据推测,胎儿骨巨噬细胞主要参与细胞碎片的吞噬和消化,但也在骨吸收过程中起作用。

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