{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T14:38:56Z","timestamp":1790692736502,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,8,2]],"date-time":"2018-08-02T00:00:00Z","timestamp":1533168000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2018,8,2]],"date-time":"2018-08-02T00:00:00Z","timestamp":1533168000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81630066"],"award-info":[{"award-number":["81630066"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["R01AR070222"],"award-info":[{"award-number":["R01AR070222"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["R01AR054465"],"award-info":[{"award-number":["R01AR054465"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:p>\n                    Osteoarthritis (OA) in the temporomandibular joint (TMJ) is a degenerative disease in the adult, which is characterized by the pathological degeneration of condylar cartilage. Axin1 plays a critical role in the regulation of cartilage development and homeostasis. To determine the role of Axin1 in TMJ tissue at the adult stage, we generated\n                    <jats:italic>Axin1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Agc1ER<\/jats:italic>\n                    <\/jats:sup>\n                    mice, in which\n                    <jats:italic>Axin1<\/jats:italic>\n                    was deleted in\n                    <jats:italic>aggrecan<\/jats:italic>\n                    \u2010expressing chondrocytes at 2 months of age. Histology, histomorphometry, and immunostaining analyses were performed using TMJ tissues harvested from 4\u2010 and 6\u2010month\u2010old mice after tamoxifen administration. Total RNA isolated from TMJ cartilage of 6\u2010month\u2010old mice was used for gene expression analysis. Progressive OA\u2010like degeneration was observed in condylar cartilage in\n                    <jats:italic>Axin1<\/jats:italic>\n                    knockout (KO) mice with loss of surface continuity and the formation of vertical fissures. In addition, reduced alcian blue staining in condylar cartilage was also found in\n                    <jats:italic>Axin1<\/jats:italic>\n                    KO mice. Immunostaining and reverse transcription quantitative polymerase chain reaction (qRT\u2010PCR) assays revealed disturbed homeostasis in condylar cartilage with increased expressions of MMP13 and Adamts5 and decreased lubricin expression in\n                    <jats:italic>Axin1<\/jats:italic>\n                    \u2010deficient chondrocytes. Less proliferative cells with increased hypertrophic and apoptotic activities were presented in the condylar cartilage of\n                    <jats:italic>Axin1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Agc1ER<\/jats:italic>\n                    <\/jats:sup>\n                    KO mice. As a scaffolding protein, the deletion of\n                    <jats:italic>Axin1<\/jats:italic>\n                    stimulated not only the \u03b2\u2010catenin but also the fibroblast growth factor (FGF) signaling via extracellular signal\u2010regulated protein kinases 1 and 2 (ERK1\/2) activation. The qRT\u2010PCR results showed an increased expression of\n                    <jats:italic>Fgfr1<\/jats:italic>\n                    in\n                    <jats:italic>Axin1<\/jats:italic>\n                    KO cartilage. Overall, the deletion of\n                    <jats:italic>Axin1<\/jats:italic>\n                    in condylar chondrocytes altered the \u03b2\u2010catenin and FGF\/ERK1\/2 signaling pathways, thus cooperatively contribute to the cartilage degeneration.\n                  <\/jats:p>","DOI":"10.1002\/jcp.27043","type":"journal-article","created":{"date-parts":[[2018,8,6]],"date-time":"2018-08-06T23:30:55Z","timestamp":1533598255000},"page":"1720-1729","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Deletion of\n                    <i>Axin1<\/i>\n                    in condylar chondrocytes leads to osteoarthritis\u2010like phenotype in temporomandibular joint via activation of \u03b2\u2010catenin and FGF signaling"],"prefix":"10.1002","volume":"234","author":[{"given":"Yachuan","family":"Zhou","sequence":"first","affiliation":[{"name":"State Key Laboratory of Oral Diseases, Department of Cariology and Endodontics National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University Chengdu China"},{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bing","family":"Shu","sequence":"additional","affiliation":[{"name":"Department of Orthopedics, Longhua Hospital Shanghai University of Traditional Chinese Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liwei","family":"Zheng","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Oral Diseases, Department of Cariology and Endodontics National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuedong","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Oral Diseases, Department of Cariology and Endodontics National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guozhi","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois"},{"name":"Department of Biology Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9854-8685","authenticated-orcid":false,"given":"Di","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Rush University Medical Center Chicago 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