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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2006.1
- 수록면
- 36 - 41 (6page)
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초록· 키워드
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Objective. The objective of this study was to examine the hypothesis that inflammatory synovial fluid from TMJ internal
derangement initiates a transient increase in intracellular calcium concentration ([Ca2+]i) in chondrocytes and the induced Ca2+
signaling affects iNOS/COX-2 gene expression patterns following exposure to inflamed synovial fluid.
Materials and Methods. Two female adult patients with symptoms of TMD who agreed to participate in the study were
selected for this study. Immortalized human juvenile costal chondrocyte C-28/I2 was grown to 80% confluency and synovial
fluids from two patients were added respectively to culture media for 24 hours at the concentration of 100ng/10ml. Confocal
laser scanning microscope (CLSM) was used to examine changes of intracellular calcium concentration ([Ca2+]i). RT-PCR was
performed to identify the expression profile of IL-1α, iNOS, COX-2.
Results. Increased [Ca2+]i was observed in chondrocytes subjected to inflamed synovial fluid compared to control cultures and
in respective cultures exposed to inflamed synovial fluids from each patient, IL-1β, COX-2 mRNA were detected. However, in
neither case iNOS mRNA was expressed. IL-1α, COX-2, and iNOS mRNA were expressed in control culture.
Conclusion. Our results show that immortalized chondrocytes cultured with inflamed synovial fluids from patients diagnosed
as disc displacement without reduction and limitation in mouth opening showed increased calcium concentration and
expression of COX-2 while inhibiting the production of iNOS, which in turn could adversely affect the chondrocytes in at least
short term by hindering physiologic role of NO against inflammatory cascades. These findings suggest that inflamed synovial
fluid may differentially regulate the transcriptomes of relevant inflammatory mediators, especially iNOS/COX-2 axis in chondrocytes
through adjusting calcium transients.
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참고문헌 (25)
참고문헌 신청
/ / Osteoclastic inhibition: anaction of nitric oxide not mediated by cyclic GMP. : 2936 ~ 2940
/ 1993 / Induction of nitric oxide synthase inhuman chondrocytes : 398 ~ 405
/ 1993 / Nitric oxide activates cyclooxygenase enzymes 90 : 7240 ~ 7244
/ 1995 / Increased intracellular Ca2+ selectivelysuppresses IL-1-induced NO production by reducing iNOSmRNA stability 129 : 1651 ~ 1657
/ 1995 / Nitric oxide production and inducible ni-tric oxide synthase expression in inflammatory arthritides 96 : 2357 ~ 2363
/ 1993 / Induction of nitric oxide synthase inhuman chondrocytes : 398 ~ 405
/ 1993 / Nitric oxide activates cyclooxygenase enzymes 90 : 7240 ~ 7244
/ 1995 / Increased intracellular Ca2+ selectivelysuppresses IL-1-induced NO production by reducing iNOSmRNA stability 129 : 1651 ~ 1657
/ 1995 / Nitric oxide production and inducible ni-tric oxide synthase expression in inflammatory arthritides 96 : 2357 ~ 2363
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