Insulin receptor expression in primary and cultured osteoclast-like cells

Insulin receptor expression in primary and cultured osteoclast-like cells
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DOI:
10.1016/s8756-3282(98)00095-7
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发表时间:
1998-09-01
期刊:
影响因子:
4.1
通讯作者:
Best, JD
Best, JD
中科院分区:
医学2区
文献类型:
--
作者:
Thomas, DM;Udagawa, N;Best, JD

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被引文献

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骨骼生长是协调的骨形成和吸收的净产物,众所周知,胰岛素通过作用于成骨细胞来刺激骨形成。目前尚不清楚破骨细胞上是否存在胰岛素受体,或者胰岛素是否调节破骨功能。在此,我们提出了成熟的单核和多核小鼠破骨细胞样细胞以及原代新生大鼠和小鼠破骨细胞表达胰岛素受体的免疫细胞化学证据。放射性标记研究表明,共培养中破骨细胞样细胞的逐渐丰富与胰岛素结合的增加有关。当体外产生的破骨细胞样细胞被接种到牙本质切片上时,胰岛素剂量依赖性地抑制凹坑的形成高达80%,这表明胰岛素在破骨细胞功能中发挥了作用。这些数据与胰岛素对骨吸收的影响是一致的,除了先前承认的对骨形成的影响外,这些作用共同导致骨的净增长,(bone 23:181-186;1998)(C)1998由Elsevier Science Inc.保留所有权利。
Skeletal growth is the net product of coordinated bone formation and resorption, Insulin is known to stimulate bone formation by actions on osteoblasts. It is not known whether insulin receptors are present on osteoclasts, or whether insulin regulates osteoclastic function. We present here immunocytochemical evidence of insulin receptor expression by mature mono- and multinucleated murine osteoclast-like cells generated in vitro, and in primary neonatal rat and mouse osteoclasts. Radiolabeled studies indicated that progressive enrichment of osteoclast-like cells in coculture was associated with increased insulin binding. When osteoclast-like cells generated in vitro were plated onto dentine slices, insulin dose-dependently inhibited pit formation by up to 80%, suggesting a role for insulin in osteoclast function. These data are consistent with an effect of insulin on bone resorption in addition to those previously recognized on bone formation, actions that together result in net bone growth, (Bone 23: 181-186; 1998) (C) 1998 by Elsevier Science Inc. All rights reserved.