https://scholars.lib.ntu.edu.tw/handle/123456789/458920
標題: | Major histocompatibility complex class II transactivator inhibits cysteine-rich 61 expression in osteoblastic cells and its implication in the pathogenesis of periapical lesions | 作者: | YUAN-LING LEE SZE-KWAN LIN Hong C.-Y. Wang J.-S. Yang H. EDDIE HSIANG HUA LAI Chen M.-H. SANG-HENG KOK |
公開日期: | 2010 | 卷: | 36 | 期: | 6 | 起(迄)頁: | 1021-1025 | 來源出版物: | Journal of Endodontics | 摘要: | Introduction: Osteoblastic expression of cysteine-rich 61 (Cyr61) correlates with the severity of periapical lesion-associated bone loss, but the regulatory mechanism of Cyr61 expression was not known. Methods: In the study we examined the effect of major histocompatibility complex class II transactivator (CIITA) on tumor necrosis factor (TNF)-α-induced Cyr61 synthesis in U2OS human osteoblastic cells by Western blot analysis. In a rat model of bacteria-induced apical periodontitis, we assessed the relation between osteoblastic expressions of CIITA/Cyr61 and disease progression by radiographic and immunohistochemistry studies. Results: We found that forced expression of CIITA suppressed Cyr61 synthesis in U2OS cells. In rat periapical lesions, osteoblastic CIITA decreased as the disease progressed, and expression of CIITA is negatively related to Cyr61 synthesis in osteoblasts. Conclusions: Our data showed that CIITA is a repressor of Cyr61 synthesis in osteoblasts, and it might play a protective role in the pathogenesis of bone resorption in apical periodontitis, possibly through down-regulating the expression of Cyr61 in osteoblasts. ? 2010 Published by Elsevier Inc. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/458920 | DOI: | 10.1016/j.joen.2010.03.009 | SDG/關鍵字: | cysteine rich protein 61; MHC class II transactivator protein; nuclear protein; transactivator protein; tumor necrosis factor alpha; cysteine rich protein 61; nuclear protein; transactivator protein; tumor necrosis factor; alveolar bone loss; animal; article; comparative study; disease course; disease model; drug antagonism; drug effect; gene; human; image processing; microbiology; osteoblast; osteoclast; pathology; pathophysiology; polyacrylamide gel electrophoresis; randomization; rat; Sprague Dawley rat; time; tooth periapical disease; tooth radiography; tumor cell line; Western blotting; antagonists and inhibitors; drug effects; osteoblast; time factor; tooth periapical disease; Alveolar Bone Loss; Animals; Blotting, Western; Cell Line, Tumor; Cysteine-Rich Protein 61; Disease Models, Animal; Disease Progression; Electrophoresis, Polyacrylamide Gel; Genes, MHC Class II; Humans; Image Processing, Computer-Assisted; Nuclear Proteins; Osteoblasts; Osteoclasts; Periapical Periodontitis; Radiography, Dental, Digital; Random Allocation; Rats; Rats, Sprague-Dawley; Time Factors; Trans-Activators; Tumor Necrosis Factor-alpha; Alveolar Bone Loss; Animals; Blotting, Western; Cell Line, Tumor; Cysteine-Rich Protein 61; Disease Models, Animal; Disease Progression; Electrophoresis, Polyacrylamide Gel; Genes, MHC Class II; Humans; Image Processing, Computer-Assisted; Nuclear Proteins; Osteoblasts; Osteoclasts; Periapical Periodontitis; Radiography, Dental, Digital; Random Allocation; Rats; Rats, Sprague-Dawley; Time Factors; Trans-Activators; Tumor Necrosis Factor-alpha |
顯示於: | 牙醫學系 |
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