{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T03:49:28Z","timestamp":1790221768480,"version":"4.1.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The role of mechanical strain and estrogen status in regulating ER\u03b1 levels in bone cells was studied in female rats. OVX is associated with decreased ER\u03b1 protein expression\/osteocyte, whereas habitual strain and artificial loading has only a small but positive effect, except on the ulna's medial surface, where artificial loading stimulates reversal of resorption to formation.<\/jats:p>\n               <jats:p>Introduction: Osteoporosis is the most widespread failure of bones' ability to match their architectural strength to their habitual load bearing. In men and women, the severity of bone loss is associated with bioavailability of estrogen. This association could result from the estrogen receptor (ER) involvement in bone cells' adaptive response to loading.<\/jats:p>\n               <jats:p>Materials and Methods: In vivo semiquantitative analysis of the amount of ER\u03b1 protein per osteocyte was performed in immuno-cytochemically stained sections from control and loaded rat ulna, as well as tibias of ovariectomy (OVX) and sham-operated female rats. In vitro, the effect of exogenous estrogen (10\u22128 M) and mechanical strain (3400 \u03bc\u03f5, 1 Hz, 600 cycles) on the expression of ER\u03b1 mRNA levels was assessed in ROS 17\/2.8 cells in monolayers using real-time PCR and ER promoter activity. ER\u03b1 translocation in response to exogenous estrogen and mechanical strain was assessed in both ROS 17\/2.8 and MLO-Y4 cells.<\/jats:p>\n               <jats:p>Results: More than 90 percent of tibial osteocytes express ER\u03b1, the level\/osteocyte being higher in cortical than cancellous bone. OVX is associated with decreased ER\u03b1 protein expression\/osteocyte, whereas in the ulna habitual strain and that caused by artificial loading had only a small but positive effect, except on the medial surface, where loading stimulates reversal of resorption to formation. In unstimulated osteocytes and osteoblasts in situ, and osteocyte-like and osteoblast-like cells in vitro, ER\u03b1 is predominantly cytoplasmic. In vitro, both strain and estrogen stimulate transient ER\u03b1 translocation to the nucleus and transient changes in ER\u03b1 mRNA. Strain but not estrogen also induces discrete membrane localization of ER\u03b1.<\/jats:p>\n               <jats:p>Conclusions: Bone cells' responses to both strain and estrogen involve ER\u03b1, but only estrogen regulates its cellular concentration. This is consistent with the hypothesis that bone loss associated with estrogen deficiency is a consequence of reduction in ER\u03b1 number\/activity associated with lower estrogen concentration reducing the effectiveness of bone cells' anabolic response to strain.<\/jats:p>","DOI":"10.1359\/jbmr.060504","type":"journal-article","created":{"date-parts":[[2006,7,26]],"date-time":"2006-07-26T13:48:00Z","timestamp":1153921680000},"page":"1297-1306","source":"Crossref","is-referenced-by-count":126,"title":["Osteocytes Use Estrogen Receptor \u03b1 to Respond to Strain but Their ER\u03b1 Content Is Regulated by Estrogen"],"prefix":"10.1093","volume":"21","author":[{"given":"Gul","family":"Zaman","sequence":"first","affiliation":[{"name":"Department of Basic Sciences, The Royal Veterinary College, University of London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen L","family":"Jessop","sequence":"additional","affiliation":[{"name":"Department of 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