PubMed · 5541153
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W A Wood. 1971. Pseudogout.. https://doi.org/10.7547/87507315-61-2-59
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PURPOSE: To study the effect of semisynthetic sulphated polysaccharides in the different calcium phosphate crystallization processes in vitro. MATERIALS AND METHODS: Crystallization of hydroxyapatite (HAP) and brushite (DCPD) in the presence and absence of 2 new semisynthetic sulphated polysaccharides (G871, G872) were defined by a constant composition technique, particle size analysis and zeta potential measurement. RESULTS: These polysaccharides demonstrated strong inhibitory effect on HAP and DCPD crystal growth and agglomeration. The increase of negative zeta potential values after addition of polysaccharides suggests the binding of these polysaccharides to HAP and DCPD crystals. CONCLUSION: We conclude that both G871 and G872 could be of potential use for calcium phosphate urolithiasis prevention in addition to their use for calcium oxalate.
OBJECTIVE: To investigate BCP (basic calcium phosphate) crystal-stimulated mitogenesis and collagenase gene transcription in primary cultures of porcine chondrocytes. METHODS: The role of protein kinases in BCP crystal-stimulated DNA synthesis was investigated using thymidine incorporation, kinase inhibitors, and protein kinase C (PKC) assays. Northern blot analysis was used to determine the levels of collagenase c-fos and c-jun message. RESULTS: BCP crystals stimulated chondrocyte proliferation in a PKC-dependent manner. Increased levels of collagenase message were preceded by an increased accumulation of c-fos, but not c-jun. CONCLUSION: BCP crystals could contribute to the abnormal chondrocyte proliferation and collagenase secretion observed in some rheumatic diseases.
The present study examined the effect of membrane cholesterol on liposome-mediated calcium phosphate precipitation in metastable aqueous solutions (2.25 mM Ca2+ and 1.5 mM inorganic phosphate) at 22 degrees C, pH 7.4 and 240 mOsm. The liposomes were prepared from 7:2:X molar mixtures of phosphatidylcholine, dicetylphosphate, and cholesterol (x = 0, 1, 5, or 9) and contained either 0 or 50 mM encapsulated phosphate. The membranes were made permeable to Ca2+ by addition of the cationophore, X-537A. Changes in external Ca2+ concentration were used as the principal monitor of the course of precipitation. Without encapsulated phosphate, 7:2:X liposomes (with or without ionophore) induced no precipitation. With 50 mM encapsulated phosphate and in the presence of ionophore, precipitation significantly depended on the cholesterol level in the membrane. At 0 and 10 mole% cholesterol, precipitate developed rapidly both within and outside the liposomes. At 35 and 50 mole% cholesterol, no observable intraliposomal precipitation occurred, and extraliposomal precipitation started only after an induction period of 24 hours. Delayed extraliposomal precipitation also took place in PO4-containing liposomes without added ionophore. In this latter case, however, cholesterol was essential for this precipitation to occur with the optimum level being around 10 mole%. Suppression of ionophore-mediated intraliposomal precipitation at higher cholesterol levels could be related to the inflexible cholesterol molecules making the membrane more rigid, thereby restricting Ca-ionophore transport. This restriction could be reversed with ethanol. Delayed extraliposomal precipitation in the absence of added ionophore (or at higher cholesterol levels in its presence) could be explained by seeding from low, unobserved levels of intraliposomal precipitate formed during slow, unfacilitated Ca2+ leakage into the liposomal interior.