{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T06:38:13Z","timestamp":1768718293642,"version":"3.49.0"},"reference-count":55,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[1998,1,1]],"date-time":"1998-01-01T00:00:00Z","timestamp":883612800000},"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":[[1998,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The colony stimulating factor 1 (CSF-1) regulates osteoclastogenesis and bone resorption. Mutations in the CSF-1 gene cause an osteopetrosis characterized by the absence of osteoclasts. Mature osteoclasts respond to CSF-1 with inhibition of bone resorption and an increment of cell spreading. Herein we demonstrate that CSF-1\u2013induced osteoclast spreading depends on the substrate the osteoclast interacts with and requires integrity of the vitronectin receptor and of the c-src proto-oncogene. Rabbit osteoclasts were allowed to attach to glass, serum, osteopontin, and bone substrates, and were treated with 10 ng\/ml human recombinant CSF-1 for 4 h. In osteoclasts plated on glass, the cytokine induced 70% inhibition of bone resorption and 1.8-fold stimulation of cell spreading, without changes in podosome expression and microfilament array. In contrast, CSF-1 induced a 2.5-fold increase of osteoclasts showing filopodia, and a 9.5-fold increase of osteoclasts presenting lamellipodia, indicating that membrane motility was required for cell spreading. Osteoclasts plated on serum substrates showed a 50% reduction of spontaneous spreading. However, in this circumstance, CSF-1 still stimulated an increase of osteoclast area. In osteoclasts cultured on osteopontin substrate or on bone slices, an inhibition of CSF-1\u2013induced osteoclast spreading was observed. To establish involvement of the vitronectin receptor and c-src proto-oncogene, cells were treated with the \u03b1v\u03b23 integrin neutralizing antibody, LM609, or c-src antisense oligonucleotides, which reduced CSF-1\u2013induced osteoclast spreading by 57% and 60%, respectively. The results demonstrate that CSF-1\u2013induced osteoclast spreading requires both the vitronectin receptor and the c-src proto-oncogene and that this action is modulated by the adhesion substrata.<\/jats:p>","DOI":"10.1359\/jbmr.1998.13.1.50","type":"journal-article","created":{"date-parts":[[2006,4,26]],"date-time":"2006-04-26T22:45:43Z","timestamp":1146091543000},"page":"50-58","source":"Crossref","is-referenced-by-count":37,"title":["Colony Stimulating Factor-1\u2013Induced Osteoclast Spreading Depends on Substrate and Requires the Vitronectin Receptor and the c-<i>src<\/i> Proto-Oncogene"],"prefix":"10.1093","volume":"13","author":[{"given":"Anna","family":"Teti","sequence":"first","affiliation":[{"name":"Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna","family":"Taranta","sequence":"additional","affiliation":[{"name":"Istituto Dermopatico dell'Immacolata, Rome, 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