DR5 and DcR2 are expressed in human lumbar intervertebral discs

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Chen, Bohua
Ma, Bin
Yang, Shang-You
Xing, Xiuhua
Gu, Run
Hu, Yougu
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Chen B, Ma B, Yang S, Xing X, Gu R, Hu Y; DR5 and DcR2 are expressed in human lumbar intervertebral discs; Spine (Phila Pa 1976). Sep.2009, V.34, No.19

STUDY DESIGN: 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. OBJECTIVE: 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). SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSION: The current results indicate that disc cells, after herniation, undergo apoptotic cell death via the DR5/TRAIL pathway.

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Lippincott, Williams & Wilkins
Book Title
Spine (Phila Pa 1976).;
;v.34, No.19
PubMed ID
1528-1159 (Electronic)
0362-2436 (Print)