Osteocyte hypoxia: a novel mechanotransduction pathway

被引:90
作者
Dodd, JS
Raleigh, JA
Gross, TS
机构
[1] Univ Cincinnati, Dept Orthopaed Surg, Cincinnati, OH 45267 USA
[2] Univ N Carolina, Sch Med, Chapel Hill, NC 27599 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1999年 / 277卷 / 03期
关键词
disuse; bone loss; bone adaptation; oxygen metabolism;
D O I
10.1152/ajpcell.1999.277.3.C598
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:C598 / C602
页数:5
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