Discipline of Pathology, School of Medical Sciences, University of Adelaide, Adelaide, SA 5005, Australia.
J Dent Res. 2010 Jan;89(1):29-33. doi: 10.1177/0022034509350708.
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.
本研究探讨了牙周病中炎症细胞的存活时间延长是否归因于肿瘤坏死因子相关凋亡诱导配体（TRAIL）诱饵受体对细胞凋亡的抑制作用，以及凋亡抑制剂（IAP）家族成员对凋亡信号转导终末阶段的抑制作用。从健康个体和慢性牙周炎患者中采集牙龈组织样本。通过免疫组织化学和 mRNA 表达水平检测 TRAIL、TRAIL 受体、TUNEL、cleaved caspase-3、xIAP 和 survivin 的表达。在患病的牙周组织中，TRAIL 和 TRAIL 诱饵受体 TRAIL R4 的表达水平更高（p < 0.005）。统计学上（p < 0.05），cleaved caspase-3 和 cleaved caspase-3 抑制剂 xIAP 和 survivin 的水平也更高。在 mRNA 水平也观察到了类似的变化。结果表明，TRAIL 诱饵受体和 cleaved caspase-3 抑制剂的高表达可能抑制了牙周炎中的细胞凋亡。
