Korean J Med.
2008 Mar;74(3):296-304.
The expression of TRAIL and its receptors in human osteoarthritic cartilages
- Affiliations
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- 1Department of Internal Medicine, Dong-A University College of Medicine, Busan, Korea. leesw@dau.ac.kr
- 2Department of Anatomy and Cell biology, Dong-A University College of Medicine, Busan, Korea.
- 3Department of Forensic Medicine, Pusan National University College of Medicine, Busan, Korea.
Abstract
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BACKGROUND/AIMS: The apoptosis of chondrocytes is assumed to be involved in the pathogenesis of osteoarthritis (OA), and the TNF related apoptosis inducing ligand (TRAIL) is thought to have a pivotal role in the apoptosis of chondrocytes. We investigated the expression of TRAIL and its receptors in human osteoarthritic cartilages.
METHODS
Human OA cartilage tissues were obtained from the medial side of the cartilage in the knee joints of 25 patients who underwent total knee replacement surgery, and the normal human cartilages of the knee joint were obtained at autopsy from seven young adults who had no history of joint diseases. The expressions of TRAIL and the death receptor were analyzed by immunohistochemistry or immunofluorscent staining. The concentration of TRAIL in the synovial fluid was measured by enzyme linked immunosorbent assay.
RESULTS
TRAIL and its receptors were expressed in the OA cartilage, but not in the normal cartilage. TUNEL staining and immunohistochemistry for TRAIL on the serial sections showed that most TRAIL positive cells were TUNEL positive. The OA joint fluid contained concentrations of TRAIL that were readily detectable (80 and 120 microgram/ppm in the synovial fluid of each, respectively). However, the synovial fluid of the knee joint obtained at autopsy from the seven young adults contained low concentrations of detectable TRAIL (0~2 microgram/ppm).
CONCLUSIONS
These results support the notion that TRAIL and its receptors are involved in the pathogenesis of human OA. A better understanding of TRAIL induced apoptosis in chondrocytes might lead to the development of a new therapeutic strategy for OA.