{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T15:38:17Z","timestamp":1780414697723,"version":"3.54.1"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2022,10,31]],"date-time":"2022-10-31T00:00:00Z","timestamp":1667174400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK075462"],"award-info":[{"award-number":["DK075462"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["asbmr.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["JBMR Plus"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Metabolic acidosis (MET) stimulates bone resorption through inhibition of osteoblast (OB) bone formation and stimulation of osteoclast (OC) bone resorption. We found that OGR1, a G protein\u2010coupled proton (H\n                    <jats:sup>+<\/jats:sup>\n                    )\u2010sensing receptor, was critical for initial H\n                    <jats:sup>+<\/jats:sup>\n                    signaling in the OB. In mice with a global deletion of OGR1, we demonstrated that loss of OGR1 impairs H\n                    <jats:sup>+<\/jats:sup>\n                    \u2010induced bone resorption, leading to increased bone density through effects on both the OB and OC. Using an OC\u2010specific deletion of OGR1, we found that MET directly activates OGR1 in the OC. To determine if the response of OGR1 to MET in the OB is independent of a response in OCs and to characterize direct activation of OGR1 in the OB, we studied female mice with an OB\u2010specific deletion of OGR1 (OB\u2010cKO) and differentiated osteoblasts derived from marrow of OB\u2010cKO and wild\u2010type (WT) mice. In OB\u2010cKO mice, we found increased bone area in both tibial and femoral cortical bone. Specific loss of OB OGR1 increased in vitro mineralization, alkaline phosphatase activity, and expression of osteoblast\u2010specific genes compared with WT with no alteration in OC activity. MET stimulation of OB\n                    <jats:italic>cox2<\/jats:italic>\n                    and\n                    <jats:italic>fgf23<\/jats:italic>\n                    gene expression was inhibited in OB\u2010cKO OB. These results indicate that MET activation of OGR1 in the OB is independent of the response in the OC and that OGR1 in both cell types is required for a complete response to MET. Characterization of the role of OGR1 in MET\u2010induced bone resorption will improve our understanding of bone loss associated with metabolic acidosis in patients with chronic kidney disease. \u00a9 2022 The Authors.\n                    <jats:italic>JBMR Plus<\/jats:italic>\n                    published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.\n                  <\/jats:p>","DOI":"10.1002\/jbm4.10691","type":"journal-article","created":{"date-parts":[[2022,10,17]],"date-time":"2022-10-17T12:08:08Z","timestamp":1666008488000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Effect of Osteoblast\u2010Specific Deletion of the Proton Receptor OGR1"],"prefix":"10.1093","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5980-5127","authenticated-orcid":false,"given":"Nancy S","family":"Krieger","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine University of Rochester School of Medicine and Dentistry  Rochester NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luojing","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine University of Rochester School of Medicine and Dentistry  Rochester NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer","family":"Becker","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine University of Rochester School of Medicine and Dentistry  Rochester NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michaela","family":"Chan","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine University of Rochester School of Medicine and Dentistry  Rochester NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David 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