共查询到20条相似文献,搜索用时 31 毫秒
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Articular calcification correlates with osteoarthritis (OA) severity but its exact role in the disease process is unclear.
In examining OA meniscal cell function, Sun and colleagues have shown recently that meniscal cells from end-stage OA subjects
can generate calcium crystals and that genes involved in calcification are upregulated in OA meniscal cells. Also, this in vitro calcium deposition by OA menisci is inhibited by phosphocitrate. This study should catalyse further work examining the pathological
contribution or otherwise of calcium crystals in OA. This would significantly aid the development of potential disease modifying
agents in OA, which are currently unavailable. 相似文献
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Sun Y Zeng XR Wenger L Cheung HS 《Biochemical and biophysical research communications》2003,312(4):1053-1059
Pathological calcifications are associated with many medical conditions including diabetes, breast cancer, and crystals-associated osteoarthritis. The deposition of calcium-containing crystals on cells induces detrimental cellular effects and speeds up the progression of associated diseases. We carried out the present study to test the hypotheses that calcium-containing crystals may stimulate the influx of other molecules existing in the extracellular fluid disturbing normal molecular signaling and that anti-calcification agent will inhibit such endocytotic process. We found that basic calcium phosphate (BCP) crystals greatly stimulated the endocytotic activity of cells by rendering the cells more permeable and that the anti-calcification agent phosphocitrate and several others inhibited the crystals-mediated endocytosis. This is the first study reporting that the endocytotic activity of cells is affected by BCP crystals and that such endocytotic activity can be inhibited by anti-calcification agents. Since calcium-containing crystals are associated with many human diseases and in many circumstances are associated with apoptotic bodies, extracellular and matrix vesicles where DNA fragments, small peptides, and minerals are released into extracellular space, the findings reported here are important for our understanding of the complex biological effects and the potential pathological role of calcium-containing crystals in crystals-associated diseases, and for the development of disease modifying agents as well. 相似文献
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Structure--activity relationship of inhibitors of hydroxyapatite formation. 总被引:2,自引:1,他引:1
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The relative abilities of some compounds to inhibit the transformation of amorphous calcium phosphate into hydroxyapatite were determined. Organic diphosphates, fructose 1,6-bisphosphate, pyrophosphate, imidodiphosphate and 3-phospholycerate all inhibited to various degrees. Strong inhibition was observed with phosphonoformate, and phosphocitrate proved to be the most powerful of the inhibitors examined. On the basis of these new findings an improved concept of the structure--activity relationship of inhibitors is proposed and mechanisms for inhibitor action are discussed. 相似文献
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I Komuro Y Katoh T Kaida Y Shibazaki M Kurabayashi E Hoh F Takaku Y Yazaki 《The Journal of biological chemistry》1991,266(2):1265-1268
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Inducible binding of a factor to the c-fos enhancer 总被引:85,自引:0,他引:85
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Shear stress-induced c-fos activation is mediated by Rho in a calcium-dependent manner 总被引:3,自引:0,他引:3
Shiu YT Li S Yuan S Wang Y Nguyen P Chien S 《Biochemical and biophysical research communications》2003,303(2):548-555
We aimed at elucidating the molecular basis of c-fos promoter activation in vascular endothelial cells (ECs) in response to shear stress, with emphases on Rho family GTPases (Rho, Cdc42, and Rac) and intracellular calcium. Dominant-negative and constitutively activated mutants of these GTPases were used to block the action of upstream signals and to activate the downstream pathways, respectively. The role of intracellular calcium was assessed with intracellular calcium chelators. Only Rho, but not Cdc42 or Rac, is involved in the shear stress induction of c-fos. This Rho-mediated shear-induction of c-fos is dependent on intracellular calcium, but not on the Rho effector p160ROCK or actin filaments. While the inhibition of p160ROCK and its ensuing disruption of actin filaments decreased the basal c-fos activity in static ECs (no flow), it did not affect the shear-inductive effect. The calcium chelator BAPTA-AM inhibits the shear-induction, as well as the static level, of c-fos activity. 相似文献
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The protection afforded by phosphocitrate, a phosphorylated polycarboxylic acid, against crystal-induced membrane damage to polymorphonuclear leukocytes was studied in vitro. Membranolysis was assessed by nitro blue tetrazolium salt reduction, lactate dehydrogenase release, and scanning electron microscopy. Phosphocitrate protected strongly against hydroxyapatite crystal-induced damage, an action attributable to crystal surface binding of phosphocitrate rather than to the membrane. The ability of phosphocitrate to prevent hydroxyapatite crystallization, together with its membrane protective effect against preformed crystals, would suggest that the compound might have a useful future role against crystal-induced arthropathies. 相似文献
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