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-α, 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.
The current study showed high expression with DR5 between the herniated and normal IVD groups and mRNA expression. There were no differences in DcR2 or mRNA levels that disc cells, after herniation, undergo apoptotic cell death via the DR5/TRAIL pathway.
From the *Department of Orthopaedic Surgery, Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong, China; †Department of Biological Sciences, Orthopaedic Research Institute (ORI), Wichita State University Wichita, Wichita, KS; and ‡Department of Hematology, The Municipal Hospital, Qingdao, Shandong, China.
Acknowledgment date: March 29, 2008. Revision date: September 22, 2008. Acceptance date: September 22, 2008.
The manuscript submitted does not contain information about medical device(s)/drug(s).
No funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.
Supported by the Chinese National Human Source Department for Oversea Scholarship Foundation (2005-1).
Address correspondence and reprint requests to Bohua Chen, MD, Department of Orthopaedic Surgery, Affiliated Hospital of Qingdao University Medical College, 19 Jiangsu Road, Qingdao, Shandong, China 266003; E-mail: firstname.lastname@example.org