Osteocyte hypoxia: a novel mechanotransduction pathway

Citation
Js. Dodd et al., Osteocyte hypoxia: a novel mechanotransduction pathway, AM J P-CELL, 46(3), 1999, pp. C598-C602
Citations number
30
Categorie Soggetti
Cell & Developmental Biology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
ISSN journal
03636143 → ACNP
Volume
46
Issue
3
Year of publication
1999
Pages
C598 - C602
Database
ISI
SICI code
0363-6143(199909)46:3<C598:OHANMP>2.0.ZU;2-9
Abstract
Osteocyte hypoxia: a novel mechanotransduction pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C598-C602, 1999.-Bone is a unique tissue in which to e xamine mechanotransduction due to its essential role in weight bearing. Wit hin bone, the osteocyte is an ideal cellular mechanotransducer candidate. B ecause osteocytes reside distant from the blood supply, their metabolic nee ds are met by a combination of passive diffusion and enhanced diffusion, ar ising when the tissue is loaded during functional activity. Therefore, we h ypothesized that depriving a bone of mechanical loading (and thus eliminati ng diffusion enhanced by loading) would rapidly induce osteocyte hypoxia. U sing the avian ulna model of disuse osteopenia, we found that 24 h of unloa ding results in significant osteocyte hypoxia (8.4 +/- 1.8%) compared with control levels (1.1 +/- 0.5%; P = 0.03). Additionally, we present prelimina ry data suggesting that a brief loading regimen is sufficient to rescue ost eocytes from this fate. The rapid onset of the observed osteocyte hypoxia, the inhibition of hypoxia by brief loading, and the cellular consequences o f oxygen deprivation are suggestive of a novel mechanotransduction pathway with implications across organ systems.