{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T04:13:01Z","timestamp":1790050381713,"version":"4.0.1"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2008,6,1]],"date-time":"2008-06-01T00:00:00Z","timestamp":1212278400000},"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":[[2008,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Introduction: Short collagen IX, the exclusive isoform expressed by osteoblasts, is synthesized through alternative transcription of the col9a1 gene. The function of short collagen IX in bone was characterized in col9a1-null mutant mice.<\/jats:p>\n               <jats:p>Materials and Methods: Trabecular bone morphometry of lumbar bones and tibias was evaluated by \u03bcCT and nondecalcified histology. Osteoblastic and osteoclastic activities were evaluated by PCR- and microarray-based gene expression assays and TRACP-5b and C-terminal telopeptide (CTX) assays, as well as in vitro using bone marrow stromal cells and splenocytes. The effect of col9a1+\/\u2212 mutation on osteoclast morphology was evaluated using RAW264.7-derived osteoclastic cells cultured on the mutant or wildtype calvarial bone substrates.<\/jats:p>\n               <jats:p>Results: Col9a1 knockout mutation caused little effects on the skeletal development; however, young adult female col9a1\u2212\/\u2212 and col9a1+\/\u2212 mice exhibited significant loss of trabecular bone. The trabecular bone architecture was progressively deteriorated in both male and female heterozygous col9a1+\/\u2212 mice while aging. The aged mutant mice also exhibited signs of thoracic kyphosis and weight loss, resembling the clinical signs of osteoporosis. The col9a1+\/\u2212 osteoblasts synthesized short col9a1 transcripts at decreased rates. Whereas bone formation activities in vitro and in vivo were not affected, the mutant osteoblast expressed the elevated ratio of RANKL\/osteoprotegerin. Increased serum TRACP-5b and CTX levels were found in col9a1+\/\u2212 mice, whose bone surface was associated with osteoclastic cells that were abnormally flattened and enlarged. The mutant and wildtype splenocytes underwent similar osteoclastogenesis in vitro; however, RAW264.7-derived osteoclastic cells, when cultured on the col9a1+\/\u2212 calvaria, widely spread over the bone surface and formed large resorption pits. The surface of col9a1+\/\u2212 calvaria was found to lack the typical nanotopography.<\/jats:p>\n               <jats:p>Conclusions: The mineralized bone matrix deficient of short collagen IX may become susceptible to osteoclastic bone resorption, possibly through a novel non\u2013cell-autonomous mechanism. The data suggest the involvement of bone collagen IX in the pathogenesis of osteoporosis.<\/jats:p>","DOI":"10.1359\/jbmr.080214","type":"journal-article","created":{"date-parts":[[2008,2,5]],"date-time":"2008-02-05T18:40:45Z","timestamp":1202236845000},"page":"837-849","source":"Crossref","is-referenced-by-count":33,"title":["Trabecular Bone Deterioration in <i>col9a1<\/i>+\/\u2212 Mice Associated With Enlarged Osteoclasts Adhered to Collagen IX\u2013Deficient Bone"],"prefix":"10.1093","volume":"23","author":[{"given":"Chiachien Jake","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Bioengineering, UCLA Henry Samueli School of Engineering and Applied Science, Los Angeles, California, USA"},{"name":"The Weintraub Center for Reconstructive Biotechnology, Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, UCLA School of Dentistry, Los Angeles, California, 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