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1.
Journal of Peking University(Health Sciences) ; (6)2003.
Article in Chinese | WPRIM | ID: wpr-554351

ABSTRACT

Objective: To characterize the expression of programmed cell death 5 (PDCD5) in normal and osteoarthritic human cartilage. Methods: Articular cartilage specimens were obtained from 20 patients with osteoarthritis and 10 with femoral neck (normal cartilage) at the time of arthroplasty. Expression of PDCD5 was detected by flow cytometry, immunofluorescence, RT-PCR and immunohistochemical analysis. Results: PDCD5 expression in osteoarthritis cartilage was significantly higher than in normal cartilage especially in the nucleus. PDCD5 positive chondrocytes were mainly observed in the superficial and deep zone of osteoarthritis tissue sections,and in contrast, in the superficial and middle regions of normal controls. Conclusion: Since apoptotic chondrocyte death occurs more frequently in osteoarthritis compared to normal cartilage and PDCD5 is an apoptosis related protein, the different expression patterns of PDCD5 in osteoarthritis and normal cartilage suggest that it might be involved in the pathogenesis of osteoarthritis.

2.
Journal of Peking University(Health Sciences) ; (6)2003.
Article in Chinese | WPRIM | ID: wpr-554123

ABSTRACT

Objective: To investigate the effects of chemokine like factor 1 (CKLF1) on proliferation and metabolism of chondrocytes. Methods: Cell culture, 3H TdR and 3H Proline incorporation methods were used. Chondrocytes were harvested from rabbit articular cartilage. First passage cells were seeded on 96 well plates. After synchronization,the medium was replaced by DMEM containing 5% FCS with various concentration of CKLF1 conditioned medium. The synthesis of mucopolysaccharide was detected by Saffraan O staining. The transcription of inducible nitricoxide synthase (iNOS) was detected by semi quantitative RT-PCR. Results: CKLF1 inhibited the DNA, collagen and mucopolysaccharide synthesis significantly, meanwhile, stimulated the transcription of iNOS. Conclusion: CKLF1 inhibits the proliferation and matrix synthesis of chondrocytes, which might be an important factor resulting in cartilage destructive lesions. CKLF1 may exert its effects on chondrocytes through iNOS pathway.

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