Osteocyte hypoxia: a novel mechanotransduction pathway
Osteocyte hypoxia: a novel mechanotransduction pathway
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DOI：
10.1152/ajpcell.1999.277.3.c598
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发表时间：
1999-09-01
影响因子：
5.5
通讯作者：
Gross, TS
中科院分区：
文献类型：
--
作者：
Dodd, JS;Raleigh, JA;Gross, TS
骨细胞缺氧：一种新的力学传导途径。Am. J.Physiol.277（Cell Physiol.46）：C598-C602，1999。骨是一种独特的组织，其中检查力学转导由于其在承重的重要作用。在骨内，骨细胞是理想的细胞力学换能器候选者。由于骨细胞远离血液供应，它们的代谢需要通过被动扩散和增强扩散的组合来满足，当组织在功能活动期间被加载时产生。因此，我们假设剥夺骨的机械负荷（从而消除负荷增强的扩散）将迅速诱导骨细胞缺氧。使用废用性骨质减少的鸟类尺骨模型，我们发现，与对照水平（1.1 +/- 0.5%; P = 0.03）相比，24小时的卸载导致显著的骨细胞缺氧（8.4 +/- 1.8%）。此外，我们目前的初步数据表明，一个简短的加载方案是足以拯救骨细胞从这种命运。所观察到的骨细胞缺氧的快速发作，通过短暂的负荷抑制缺氧，以及缺氧的细胞后果提示了一种新的机械转导途径，其影响跨越器官系统。
Osteocyte hypoxia: a novel mechanotransduction pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C598-C602, 1999.-Bone is a unique tissue in which to examine mechanotransduction due to its essential role in weight bearing. Within bone, the osteocyte is an ideal cellular mechanotransducer candidate. Because osteocytes reside distant from the blood supply, their metabolic needs are met by a combination of passive diffusion and enhanced diffusion, arising when the tissue is loaded during functional activity. Therefore, we hypothesized that depriving a bone of mechanical loading (and thus eliminating diffusion enhanced by loading) would rapidly induce osteocyte hypoxia. Using the avian ulna model of disuse osteopenia, we found that 24 h of unloading results in significant osteocyte hypoxia (8.4 +/- 1.8%) compared with control levels (1.1 +/- 0.5%; P = 0.03). Additionally, we present preliminary data suggesting that a brief loading regimen is sufficient to rescue osteocytes from this fate. The rapid onset of the observed osteocyte hypoxia, the inhibition of hypoxia by brief loading, and the cellular consequences of oxygen deprivation are suggestive of a novel mechanotransduction pathway with implications across organ systems.