Murray E J, Tram K K, Spencer M J, Tidball J G, Murray S S, Lee D B
Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, Sepulveda, Calif., USA.
Miner Electrolyte Metab. 1995;21(1-3):184-8.
Parathyroid hormone (PTH)-induced osteoblast retraction may play a pivotal role a role in bone resorption by providing osteoclasts direct access to mineralized bone surface. We have been working on the hypothesis that the calpains participate in this retractile response through a calcium-dependent process. We have first demonstrated the presence of calpain activities in MC3T3-E1 osteoblastic cells and that these activities can be stimulated by PTH. Second, we have demonstrated that the PTH-induced osteoblast retraction is dramatically attenuated by two different cysteine protease inhibitors. Finally, initial immunofluorescent cytochemical studies suggest that this PTH-induced osteoblastic retraction is mediated through a calpain-dependent, proteolytic modification of the cytoskeletal organization.
甲状旁腺激素（PTH）诱导的成骨细胞收缩可能通过为破骨细胞提供直接接触矿化骨表面的途径，在骨吸收中起关键作用。我们一直致力于研究这样一个假说，即钙蛋白酶通过钙依赖过程参与这种收缩反应。我们首先证明了MC3T3-E1成骨细胞中存在钙蛋白酶活性，并且这些活性可被PTH刺激。其次，我们证明了两种不同的半胱氨酸蛋白酶抑制剂可显著减弱PTH诱导的成骨细胞收缩。最后，初步的免疫荧光细胞化学研究表明，这种PTH诱导的成骨细胞收缩是通过钙蛋白酶依赖的细胞骨架组织蛋白水解修饰介导的。
