Inhibition of Apoptosis in Periodontitis

被引:48
作者
Lucas, H. [1 ]
Bartold, P. M. [2 ]
Dharmapatni, A. A. S. S. K. [1 ]
Holding, C. A. [1 ]
Haynes, D. R. [1 ]
机构
[1] Univ Adelaide, Sch Med Sci, Discipline Pathol, Adelaide, SA 5005, Australia
[2] Colgate Australian Clin Dent Res Ctr, Adelaide, SA, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
apoptosis; TRAIL; caspase-3; xIAP; survivin; B LIGAND RANKL; RHEUMATOID-ARTHRITIS; DEATH DOMAIN; IN-VITRO; RECEPTOR; EXPRESSION; TRAIL; INFLAMMATION; DISEASES; FAMILY;
D O I
10.1177/0022034509350708
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.
引用
收藏
页码:29 / 33
页数:5
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