Chen Bohua, Ma Bin, Yang Shangyou, Xing Xiuhua, Gu Run, Hu Yougu
Department of Orthopaedic Surgery, Affiliated Hospital of Qingdao University Medical College, Shandong, China.
Spine (Phila Pa 1976). 2009 Sep 1;34(19):E677-81. doi: 10.1097/BRS.0b013e3181b4d4ee.
To conform the 3 media way of the apoptosis for the degenerative lumbar disc with DR5 (TRAIL-R2) and DcR2 (TRAIL-R4), as one of the tumor necrosis factors family.
To detect the expression of the DR5 (TRAIL-R2) and DcR2 (TRAIL-R4) protein and mRNA in human herniated and normal lumbar intervertebral discs (IVD).
The pathogenesis of lumber intervertebral disc herniation and degeneration is still unclear. A series of reports have suggested that apoptosis may play a key role in intervertebral disc degeneration. There are 3 apoptosis-inducing factors: FasL, TNF-alpha, and TRAIL, which trigger cell death by apoptosis-signaling pathways. These factors combined with the ligand to induce apoptosis. We have reported the expression of DR4 in IVD before. To our knowledge, there are still no studies the important role of the DR5 and DcR2 for apoptosis in IVD tissue.
The expression and distribution of DR5 and DcR2 proteins were assessed using immunostaining in 60 herniated lumbar IVD and 22 normal lumbar IVD tissue samples. DR5 and DcR2 mRNA was also quantified using real time fluorescent reverse transcriptase-polymerase chain reaction (RT-PCR) in 30 herniated lumbar IVD and 9 normal lumbar IVD.
There were significant differences in the percentage of samples with DR5 expression between the herniated (41.60%) and normal IVD (26.09%) groups (P = 0.001). Similarly, DR5 mRNA levels differed between groups (P = 0.025). However, there were no differences in DcR2 protein or mRNA levels.
The current results indicate that disc cells, after herniation, undergo apoptotic cell death via the DR5/TRAIL pathway.
作为肿瘤坏死因子家族之一，通过死亡受体5（DR5，肿瘤坏死因子相关凋亡诱导配体受体2，TRAIL-R2）和诱捕受体2（DcR2，肿瘤坏死因子相关凋亡诱导配体受体4，TRAIL-R4）来确定退变腰椎间盘细胞凋亡的三种介质途径。
检测人腰椎间盘突出症患者和正常腰椎间盘组织中DR5（TRAIL-R2）和DcR2（TRAIL-R4）蛋白及mRNA的表达。
腰椎间盘突出症和退变的发病机制仍不清楚。一系列报告表明，细胞凋亡可能在椎间盘退变中起关键作用。有三种凋亡诱导因子：FasL、肿瘤坏死因子-α（TNF-α）和肿瘤坏死因子相关凋亡诱导配体（TRAIL），它们通过凋亡信号通路触发细胞死亡。这些因子与配体结合诱导细胞凋亡。我们之前已报道了DR4在椎间盘组织中的表达。据我们所知，目前尚无关于DR5和DcR2在椎间盘组织细胞凋亡中重要作用的研究。
采用免疫染色法评估60例腰椎间盘突出症患者和22例正常腰椎间盘组织样本中DR5和DcR2蛋白的表达及分布情况。同时，采用实时荧光逆转录聚合酶链反应（RT-PCR）对30例腰椎间盘突出症患者和9例正常腰椎间盘组织样本中的DR5和DcR2 mRNA进行定量分析。
腰椎间盘突出症组（41.60%）和正常椎间盘组（26.09%）之间DR5表达阳性样本百分比存在显著差异（P = 0.001）。同样，两组间DR5 mRNA水平也存在差异（P = 0.025）。然而，DcR2蛋白或mRNA水平在两组间无差异。
目前结果表明，椎间盘突出后，椎间盘细胞通过DR5/TRAIL途径发生凋亡性细胞死亡。
