Liu Peihong, Zhang Hua, Liu Chao, Wang Xiaofang, Chen Li, Qin Chunlin
Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
PLoS One. 2014 Dec 5;9(12):e114396. doi: 10.1371/journal.pone.0114396. eCollection 2014.
FAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.
By crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.
The cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.
Loss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.
FAM20C是一种可使分泌蛋白磷酸化的激酶。先前的研究表明，FAM20C在骨、牙本质和牙釉质的形成及矿化过程中发挥着重要作用。本研究分析了FAM20C功能丧失对小鼠牙周组织健康的影响。
通过将2.3 kb Col 1a1-Cre小鼠与Fam20Cfl/fl小鼠杂交，我们构建了2.3 kb Col 1a1-Cre;Fam20Cfl/fl（cKO）小鼠，其中Fam20C在表达I型胶原蛋白的细胞中失活。我们使用X射线摄影、组织学、扫描电子显微镜和免疫组织化学方法分析了cKO小鼠的牙周组织。
cKO小鼠出现了明显的牙槽骨和牙骨质丧失，同时伴有牙周韧带炎症和牙周袋形成。cKO小鼠牙槽骨中的骨细胞和陷窝-小管网络显示出明显异常。在Fam20C缺陷的牙槽骨和/或牙骨质中，骨唾液蛋白、骨桥蛋白、牙本质基质蛋白1和牙本质涎蛋白水平降低，而在cKO小鼠的牙周韧带中，骨膜蛋白和原纤维蛋白-1减少。
Fam20C功能丧失导致小鼠牙周疾病。骨唾液蛋白、骨桥蛋白、牙本质基质蛋白1、牙本质涎蛋白、骨膜蛋白和原纤维蛋白-1水平降低可能导致Fam20C缺陷小鼠出现牙周缺陷。
