{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T08:37:22Z","timestamp":1778661442308,"version":"3.51.4"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T00:00:00Z","timestamp":1510876800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR\u201044741"],"award-info":[{"award-number":["AR\u201044741"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DE\u2010023813"],"award-info":[{"award-number":["DE\u2010023813"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR\u2010070135"],"award-info":[{"award-number":["AR\u2010070135"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,4,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>CCAAT\/enhancer-binding protein \u03b1 (C\/ebp\u03b1) is critical for osteoclastogenesis by regulating osteoclast (OC) lineage commitment and is also important for OC differentiation and function in vitro. However, the role of C\/ebp\u03b1 in postnatal skeletal development has not been reported owing to lethality in C\/ebp\u03b1\u2013\/\u2013 mice from hypoglycemia within 8 hours after birth. Herein, we generated conditional knockout mice by deleting the C\/ebp\u03b1 gene in monocyte via LysM-Cre to examine its role in OC differentiation and function. C\/ebp\u03b1f\/fLysM-Cre mice exhibited postnatal osteopetrosis due to impaired osteoclastogenesis, OC lineage priming defects, as well as defective OC differentiation and activity. Furthermore, our ex vivo analysis demonstrated that C\/ebp\u03b1 conditional deletion significantly reduced OC differentiation, maturation, and activity while mildly repressing macrophage development. At the molecular level, C\/ebp\u03b1 deficiency significantly suppresses the expressions of OC genes associated with early stages of osteoclastogenesis as well as genes associated with OC differentiation and activity. We also identified numerous C\/ebp\u03b1 critical cis-regulatory elements on the Cathepsin K promoter that allow C\/ebp\u03b1 to significantly upregulate Cathepsin K expression during OC differentiation and activity. In pathologically induced mouse model of osteoporosis, C\/ebp\u03b1 deficiency can protect mice against ovariectomy-induced bone loss, uncovering a central role for C\/ebp\u03b1 in osteolytic diseases. Collectively, our findings have further established C\/ebp\u03b1 as a promising therapeutic target for bone loss by concurrently targeting OC lineage priming, differentiation, and activity. \u00a9 2017 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.3342","type":"journal-article","created":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T16:32:36Z","timestamp":1510936356000},"page":"691-703","source":"Crossref","is-referenced-by-count":16,"title":["Monocyte-Specific Knockout of C\/ebp\u03b1 Results in Osteopetrosis Phenotype, Blocks Bone Loss in Ovariectomized Mice, and Reveals an Important Function of C\/ebp\u03b1 in Osteoclast Differentiation and Function"],"prefix":"10.1093","volume":"33","author":[{"given":"Wei","family":"Chen","sequence":"first","affiliation":[{"name":"Department of PathologyUniversity of AlabamaBirminghamALUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guochun","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of PathologyUniversity of AlabamaBirminghamALUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joel","family":"Jules","sequence":"additional","affiliation":[{"name":"Department of PathologyUniversity of AlabamaBirminghamALUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diep","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Department of PathologyUniversity of AlabamaBirminghamALUSA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yi-Ping","family":"Li","sequence":"additional","affiliation":[{"name":"Department of PathologyUniversity of 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