Article

Major histocompatibility complex class II transactivator inhibits cysteine-rich 61 expression in osteoblastic cells and its implication in the pathogenesis of periapical lesions.

Graduate Institute of Clinical Dentistry, School of Dentistry, College of Medicine, National Taiwan University, Taipei, Taiwan.
Journal of endodontics (impact factor: 2.95). 06/2010; 36(6):1021-5. DOI:10.1016/j.joen.2010.03.009 pp.1021-5
Source: PubMed

ABSTRACT 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.
In the study we examined the effect of major histocompatibility complex class II transactivator (CIITA) on tumor necrosis factor (TNF)-alpha-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.
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.
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.

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Keywords

apical periodontitis
 
bacteria-induced apical periodontitis
 
CIITA
 
CIITA suppressed Cyr61 synthesis
 
Cyr61 synthesis
 
disease progressed
 
disease progression
 
immunohistochemistry studies
 
major histocompatibility complex class II transactivator
 
osteoblastic CIITA
 
Osteoblastic expression
 
osteoblastic expressions
 
periapical lesion-associated bone loss
 
rat model
 
rat periapical lesions
 
regulatory mechanism
 
TNF)-alpha-induced Cyr61 synthesis
 
tumor necrosis factor
 
U2OS human osteoblastic cells
 
Western blot analysis