{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:21:14Z","timestamp":1784557274852,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,7,1]]},"abstract":"<jats:p>\n                    G\n                    <jats:sub>S<\/jats:sub>\n                    , the stimulatory heterotrimeric G protein, is an essential regulator of osteogenesis and bone turnover. To determine if increasing G\u03b1\n                    <jats:sub>S<\/jats:sub>\n                    in osteoblasts alters bone responses to hyperparathyroidism, we used a transgenic mouse line overexpressing G\u03b1\n                    <jats:sub>S<\/jats:sub>\n                    in osteoblasts (G\n                    <jats:sub>S<\/jats:sub>\n                    -Tg mice). Primary osteoblasts from G\n                    <jats:sub>S<\/jats:sub>\n                    -Tg mice showed increased basal and parathyroid hormone (PTH)-stimulated cAMP and greater responses to PTH than cells from WT mice. Skeletal responses to 2-week continuous PTH administration (cPTH) in female mice resulted in trabecular bone loss in WT mice but 74% and 34% increase in trabecular bone mass in long bones and vertebrae, respectively, in G\n                    <jats:sub>S<\/jats:sub>\n                    -Tg mice. Vertebral biomechanical strength was compromised by cPTH treatment in WT mice but not in G\n                    <jats:sub>S<\/jats:sub>\n                    -Tg. Increased peritrabecular fibrosis was greatly increased by cPTH in G\n                    <jats:sub>s<\/jats:sub>\n                    -Tg compared to WT mice and corresponded with greater increases in Wnt pathway proteins in trabecular bone. Cortical bone responded negatively to cPTH in WT and G\n                    <jats:sub>s<\/jats:sub>\n                    -Tg mice with large increases in porosity, decreased cortical thickness and compromised biomechanical properties. These results demonstrate that hyperparathyroidism can increase trabecular bone when G\n                    <jats:sub>S<\/jats:sub>\n                    expression and cAMP stimulation in osteoblasts are increased but this is not the case in cortical bone where increased G\n                    <jats:sub>S<\/jats:sub>\n                    expression exacerbates cortical bone loss.\n                  <\/jats:p>","DOI":"10.1530\/joe-22-0045","type":"journal-article","created":{"date-parts":[[2022,5,31]],"date-time":"2022-05-31T06:42:57Z","timestamp":1653979377000},"page":"13-26","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":3,"title":["Increased osteoblast G\u03b1S level determines bone response to hyperparathyroidism in female mice"],"prefix":"10.1530","volume":"254","author":[{"given":"Lucia","family":"Zhang","sequence":"first","affiliation":[{"name":"1Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada"},{"name":"2Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathy K","family":"Lee","sequence":"additional","affiliation":[{"name":"1Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada"},{"name":"2Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kim S","family":"Sugamori","sequence":"additional","affiliation":[{"name":"1Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc D","family":"Grynpas","sequence":"additional","affiliation":[{"name":"2Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1001-7490","authenticated-orcid":true,"given":"Jane","family":"Mitchell","sequence":"additional","affiliation":[{"name":"1Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/joe.bioscientifica.com\/view\/journals\/joe\/254\/1\/JOE-22-0045.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/joe.bioscientifica.com\/downloadpdf\/journals\/joe\/254\/1\/JOE-22-0045.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:57:41Z","timestamp":1784555861000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/joe\/article\/254\/1\/13-26\/5517"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022,7,1]]},"references-count":0,"journal-issue":{"issue":"1"},"URL":"https:\/\/doi.org\/10.1530\/joe-22-0045","relation":{},"ISSN":["0022-0795","1479-6805"],"issn-type":[{"value":"0022-0795","type":"print"},{"value":"1479-6805","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022,7,1]]}}}