{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T12:57:08Z","timestamp":1760101028423,"version":"3.40.4"},"reference-count":28,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2018,2,28]],"date-time":"2018-02-28T00:00:00Z","timestamp":1519776000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81502902","81703576"],"award-info":[{"award-number":["81502902","81703576"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Identification of agents that inhibit osteoclast formation and function is important for the treatment of osteolytic diseases which feature excessive osteoclast formation and bone resorption. Latanoprost (LTP), an analog of prostaglandin F2\u03b1, is a medication which works to lower pressure inside the eyes. Prostaglandin F2\u03b1 was reported to regulate bone metabolism, however, the effect of LTP in osteoclastogenesis is still unknown. Here, we found that LTP suppressed RANKL\u2010induced osteoclastogenesis in a dose\u2010dependent manner as illustrated by TRAP activity and TRAP staining. In addition, the osteoclast function was also reduced by LTP treatment, as indicated in less osteoclastic resorption pit areas. Furthermore, LTP inhibited the mRNA expressions of osteoclast marker genes such as TRAP and cathepsin K. In order to illustrate its molecular mechanism, we examined the changing of mRNA and protein levels of NFATc1 and c\u2010fos by LTP treatment, as well as the phosphorylation of ERK, AKT, JNK, and p38. The results suggested that LTP inhibited RANKL\u2010induced osteoclastgenesis and function by inhibiting ERK, AKT, JNK, and p38 cascade, following by the c\u2010fos\/NFATc1 pathway. In agreement with in vitro results, using an in vivo lipopolysaccharide\u2010induced murine calvaria osteolysis mouse model, we found that administration of LTP was able to reverse the lipopolysaccharide\u2010induced bone loss. Together, these data demonstrated that LTP attenuated the bone loss in lipopolysaccharide\u2010induced murine calvaria osteolysis mice through inhibiting osteoclast formation and function. Our study thus provided the evidences that LTP was a potential treatment option against osteolytic bone diseases.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26646","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T11:13:41Z","timestamp":1514114021000},"page":"4680-4691","source":"Crossref","is-referenced-by-count":6,"title":["The prevention of latanoprost on osteoclastgenesis in vitro and lipopolysaccharide\u2010induced murine calvaria osteolysis in vivo"],"prefix":"10.1002","volume":"119","author":[{"given":"Xing","family":"Xu","sequence":"first","affiliation":[{"name":"Shanghai Key Laboratory for Bone and Joint Diseases Shanghai Institute of Traumatology and Orthopedics Shanghai Ruijin Hospital Shanghai Jiaotong University School of Medicine Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yufei","family":"Yan","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory for Bone and Joint Diseases 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