The expression of TRAIL and its receptors in human osteoarthritic cartilages.
- Author:
Sang Yeob LEE
1
;
Jeong Mo KOO
;
Hyun Seung YOO
;
Young Hoon KIM
;
Ja Won KIM
;
Jae Hoon LEE
;
Hyun Jong HONG
;
Hye In KIM
;
Su Kyung PARK
;
Sung Won LEE
;
Won Tae CHUNG
;
Young Hyun YOO
;
Gi Yeong HUH
Author Information
1. Department of Internal Medicine, Dong-A University College of Medicine, Busan, Korea. leesw@dau.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Chondrocytes;
Osteoarthritis;
TRAIL
- MeSH:
Apoptosis;
Arthroplasty, Replacement, Knee;
Autopsy;
Cartilage;
Chondrocytes;
Enzyme-Linked Immunosorbent Assay;
Humans;
Immunohistochemistry;
In Situ Nick-End Labeling;
Joint Diseases;
Joints;
Knee Joint;
Osteoarthritis;
Synovial Fluid;
TNF-Related Apoptosis-Inducing Ligand;
Young Adult
- From:Korean Journal of Medicine
2008;74(3):296-304
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
