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猪软骨细胞无机焦磷酸生成的转导机制。

Transduction mechanisms of porcine chondrocyte inorganic pyrophosphate elaboration.

作者信息

Ryan L M, Kurup I V, Cheung H S

机构信息

University of Miami School of Medicine, and Department of Veterans Affairs Medical Center, Florida, USA.

出版信息

Arthritis Rheum. 1999 Mar;42(3):555-60. doi: 10.1002/1529-0131(199904)42:3<555::AID-ANR21>3.0.CO;2-Z.

Abstract

OBJECTIVE

To investigate cellular signaling mechanisms that influence chondrocyte production of inorganic pyrophosphate (PPi), which promotes calcium pyrophosphate dihydrate (CPPD) crystal deposition.

METHODS

Articular chondrocyte and cartilage cultures were stimulated with protein kinase C (PKC) activator and adenyl cyclase activator. Generation of extracellular PPi was measured.

RESULTS

Adenyl cyclase activation resulted in diminished pyrophosphate generation. PKC activation stimulated pyrophosphate elaboration.

CONCLUSION

Two signaling pathways, cAMP and PKC, modulate generation of extracellular pyrophosphate by cartilage and chondrocytes. They are novel targets for potentially diminishing extracellular pyrophosphate elaboration that leads to CPPD crystal deposition.

摘要

目的

研究影响软骨细胞产生无机焦磷酸(PPi)的细胞信号传导机制,PPi可促进二水焦磷酸钙(CPPD)晶体沉积。

方法

用蛋白激酶C(PKC)激活剂和腺苷酸环化酶激活剂刺激关节软骨细胞和软骨培养物。测量细胞外PPi的生成量。

结果

腺苷酸环化酶激活导致焦磷酸生成减少。PKC激活刺激焦磷酸生成。

结论

两条信号通路,即环磷酸腺苷(cAMP)和PKC,调节软骨和软骨细胞细胞外焦磷酸的生成。它们是潜在减少导致CPPD晶体沉积的细胞外焦磷酸生成的新靶点。

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