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The Effect of In Vivo Mechanical Loading on Estrogen Receptor α Expression in Rat Ulnar Osteocytes
Author(s) -
Ehrlich P. J.,
Noble B. S.,
Jessop H. L.,
Stevens H. Y.,
Mosley J. R.,
Lanyon L. E.
Publication year - 2002
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2002.17.9.1646
Subject(s) - endocrinology , in vivo , medicine , estrogen receptor , strain (injury) , population , alpha (finance) , estrogen receptor alpha , estrogen , biology , chemistry , anatomy , surgery , construct validity , microbiology and biotechnology , environmental health , cancer , breast cancer , patient satisfaction
The presence of estrogen receptor α (ERα) in osteocytes was identified immunocytochemically in transverse sections from 560 to 860 μm distal to the midshaft of normal neonatal and adult male and female rat ulnas ( n = 3 of each) and from adult male rat ulnas that had been exposed to 10 days of in vivo daily 10‐minute periods of cyclic loading producing peak strains of either −3000 ( n = 3) or −4000 microstrain ( n = 5). Each animal ambulated normally between loading periods, and its contralateral ulna was used as a control. In animals in which limbs were subject to normal locomotor loading alone, 14 ±1.2% SEM of all osteocytes in each bone section were ERα positive. There was no influence of either gender ( p = 0.725) or age ( p = 0.577) and no interaction between them ( p = 0.658). In bones in which normal locomotion was supplemented by short periods of artificial loading, fewer osteocytes expressed ERα (7.5 ± 0.91% SEM) than in contralateral control limbs, which received locomotor loading alone (14 ± 1.68% SEM; p = 0.01; median difference, 6.43; 95% CI, 2.60, 10.25). The distribution of osteocytes expressing ERα was uniform across all sections and thus did not reflect local peak strain magnitude. This suggests that osteocytes respond to strain as a population, rather than as individual strain‐responsive cells. These data are consistent with the hypothesis that ERα is involved in bone cells' responses to mechanical strain. High strains appear to decrease ERα expression. In osteoporotic bone, the high strains assumed to accompany postmenopausal bone loss may reduce ERα levels and therefore impair the capacity for appropriate adaptive remodeling.