Ryan L M, Kurup I, McCarty D J, Cheung H S
Department of Medicine, Medical College of Wisconsin, Milwaukee 53226.
Arthritis Rheum. 1990 Feb;33(2):235-40. doi: 10.1002/art.1780330212.
Inorganic pyrophosphate (PPi), a product of glycosaminoglycan synthesis, may be cosecreted with matrix proteoglycan to reach the extracellular site where calcium pyrophosphate dihydrate crystals form. To test this hypothesis, sulfated glycosaminoglycan synthesis by articular cartilage in culture was stimulated or inhibited while the effect on extracellular PPi was measured. When stimulated by 0.8 mM xyloside to increase 35SO4 incorporation (mean +/- SEM % of control 183 +/- 16, n = 5), PPi accumulation changed little (from 54 +/- 6 pmoles/mg to 63 +/- 8 pmoles/mg of cartilage wet weight). Inhibition of sulfation with monensin or diethylcarbamazine disproportionately lowered 35SO4 incorporation compared with PPi elaboration. Using 60 mM diethylcarbamazine, PPi production was preserved (105 +/- 8% mean +/- SEM) compared with control cultures, while sulfation was markedly inhibited (7 +/- 1%). This dissociation of sulfate incorporation and PPi secretion indicates that it is not likely that glycosaminoglycan sulfation is the source of the PPi that escapes from chondrocytes to participate in the formation of extracellular crystals.
无机焦磷酸（PPi）是糖胺聚糖合成的产物，可能与基质蛋白聚糖共同分泌至细胞外部位，焦磷酸钙二水合物晶体在此处形成。为验证这一假设，在培养过程中刺激或抑制关节软骨硫酸化糖胺聚糖的合成，同时测定对细胞外PPi的影响。当用0.8 mM木糖昔刺激以增加35SO4掺入量时（对照组的平均值±标准误为183±16%，n = 5），PPi积累变化不大（从54±6皮摩尔/毫克软骨湿重增至63±8皮摩尔/毫克软骨湿重）。与PPi生成相比，莫能菌素或二乙氨基甲嗪抑制硫酸化使35SO4掺入量降低得更多。使用60 mM二乙氨基甲嗪时，与对照培养物相比，PPi生成得以保留（平均值±标准误为105±8%），而硫酸化则受到显著抑制（7±1%）。硫酸掺入与PPi分泌的这种分离表明，糖胺聚糖硫酸化不太可能是从软骨细胞逸出并参与细胞外晶体形成的PPi的来源。
