{"title":"mmp -2缺陷小鼠下颌髁I型和II型胶原蛋白、聚集蛋白、MMP-9和MMP-13的免疫组织化学表征","authors":"Mu-Chen Yang, Megumi Nakamura, Miyuki Mayanagi, Yasuyuki Sasano","doi":"10.2220/biomedres.44.65","DOIUrl":null,"url":null,"abstract":"<p><p>Mice devoid of matrix metalloproteinase (MMP)-2 due to gene targeting have been reported to show articular cartilage destruction in the knee joint; however, the phenotype of the mandibular condylar cartilage remains unknown. Thus, in the present study, we investigated the mandibular condyle in Mmp2<sup>-/-</sup> mice. We obtained and bred Mmp2<sup>-/-</sup> mice from the same source as the previous study, and performed genotyping using genomic DNA extracted from finger snips. The mandibular condyle of Mmp2<sup>-/-</sup> mice and wild-type (WT) mice was immunohistochemically examined for the localization of extracellular matrix (ECM) proteins (type I and II collagen, and aggrecan), and MMP-9 and MMP-13. No cartilage destruction was observed in the mandibular condyle of Mmp2<sup>-/-</sup> mice, and no difference was found in the localization of the ECM proteins between the Mmp2<sup>-/-</sup> mice and WT mice. However, the bone marrow cavity in the subchondral bone of the mandibular condyle was more distinct in Mmp2<sup>-/-</sup> mice than in WT mice at the age of 50 weeks. Of note, MMP-9 characteristically localized in multinucleated cells in the mandibular condyle in 50-week-old Mmp2<sup>-/-</sup> mice. MMP-2 may be involved in the regulation of osteoclast differentiation and the formation of the bone marrow cavity in aged mice.</p>","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":null,"pages":null},"PeriodicalIF":1.3000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Immunohistochemical characterization of the mandibular condyle for type I and II collagen, aggrecan, MMP-9, and MMP-13 in MMP-2-deficient mice.\",\"authors\":\"Mu-Chen Yang, Megumi Nakamura, Miyuki Mayanagi, Yasuyuki Sasano\",\"doi\":\"10.2220/biomedres.44.65\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Mice devoid of matrix metalloproteinase (MMP)-2 due to gene targeting have been reported to show articular cartilage destruction in the knee joint; however, the phenotype of the mandibular condylar cartilage remains unknown. Thus, in the present study, we investigated the mandibular condyle in Mmp2<sup>-/-</sup> mice. We obtained and bred Mmp2<sup>-/-</sup> mice from the same source as the previous study, and performed genotyping using genomic DNA extracted from finger snips. The mandibular condyle of Mmp2<sup>-/-</sup> mice and wild-type (WT) mice was immunohistochemically examined for the localization of extracellular matrix (ECM) proteins (type I and II collagen, and aggrecan), and MMP-9 and MMP-13. No cartilage destruction was observed in the mandibular condyle of Mmp2<sup>-/-</sup> mice, and no difference was found in the localization of the ECM proteins between the Mmp2<sup>-/-</sup> mice and WT mice. However, the bone marrow cavity in the subchondral bone of the mandibular condyle was more distinct in Mmp2<sup>-/-</sup> mice than in WT mice at the age of 50 weeks. Of note, MMP-9 characteristically localized in multinucleated cells in the mandibular condyle in 50-week-old Mmp2<sup>-/-</sup> mice. MMP-2 may be involved in the regulation of osteoclast differentiation and the formation of the bone marrow cavity in aged mice.</p>\",\"PeriodicalId\":9138,\"journal\":{\"name\":\"Biomedical Research-tokyo\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical Research-tokyo\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2220/biomedres.44.65\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical Research-tokyo","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2220/biomedres.44.65","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Immunohistochemical characterization of the mandibular condyle for type I and II collagen, aggrecan, MMP-9, and MMP-13 in MMP-2-deficient mice.
Mice devoid of matrix metalloproteinase (MMP)-2 due to gene targeting have been reported to show articular cartilage destruction in the knee joint; however, the phenotype of the mandibular condylar cartilage remains unknown. Thus, in the present study, we investigated the mandibular condyle in Mmp2-/- mice. We obtained and bred Mmp2-/- mice from the same source as the previous study, and performed genotyping using genomic DNA extracted from finger snips. The mandibular condyle of Mmp2-/- mice and wild-type (WT) mice was immunohistochemically examined for the localization of extracellular matrix (ECM) proteins (type I and II collagen, and aggrecan), and MMP-9 and MMP-13. No cartilage destruction was observed in the mandibular condyle of Mmp2-/- mice, and no difference was found in the localization of the ECM proteins between the Mmp2-/- mice and WT mice. However, the bone marrow cavity in the subchondral bone of the mandibular condyle was more distinct in Mmp2-/- mice than in WT mice at the age of 50 weeks. Of note, MMP-9 characteristically localized in multinucleated cells in the mandibular condyle in 50-week-old Mmp2-/- mice. MMP-2 may be involved in the regulation of osteoclast differentiation and the formation of the bone marrow cavity in aged mice.
期刊介绍:
Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..