{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T01:36:55Z","timestamp":1791077815026,"version":"4.1.0"},"reference-count":17,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,9,21]],"date-time":"2013-09-21T00:00:00Z","timestamp":1379721600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Mice lacking ADAM10 in endothelial cells (<jats:italic>Adam10\u0394EC<\/jats:italic> mice) have shorter femurs, tibiae, and humeri than controls, raising questions about how endothelial cells could control long bone growth. We performed a histopathological evaluation of the femur and tibia growth plates at different postnatal stages, and assessed the distribution of TRAP\u2010positive osteoclasts and endothelial cells at the growth plate. The growth plates in <jats:italic>Adam10\u0394EC<\/jats:italic> mice appeared normal at P7 and P14, but a thickened zone of hypertrophic chondrocytes and increased trabecular bone density were apparent by P21 and later. The number of TRAP+ cells at the COJ was normal at P7 and P14, but was strongly reduced at P21 and later. Moreover, the density of endomucin\u2010stained endothelial cells at the COJ was increased starting at P7. The defects in long bone growth in <jats:italic>Adam10\u0394EC<\/jats:italic> mice could be caused by a lack of osteoclastogenesis at the COJ. Moreover, ADAM10 appears to regulate endothelial cell organization in the developing bone vasculature, perhaps in a similar manner as in the developing retinal vascular tree, where ADAM10 is thought to control Notch\u2010dependent endothelial cell fate decisions. This study provides evidence for the regulation of osteoclast function by endothelial cells in vivo. \u00a9 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Hill","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program New York New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary B.","family":"Goldring","sequence":"additional","affiliation":[{"name":"Tissue Engineering Regeneration and Repair Program The Hospital for Special Surgery New York New York 10021"},{"name":"Department of Cell and Developmental Biology Weill Cornell Medical College New York New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krzysztof","family":"Glomski","sequence":"additional","affiliation":[{"name":"Arthritis and Tissue Degeneration Program New York New York 10021"},{"name":"Department of Cell and Developmental Biology Weill Cornell Medical College New York New York 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carl 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