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首页> 外文期刊>Journal of Cellular Physiology >Nongenomic regulation of protein kinase C isoforms by the vitamin D metabolites 1 alpha,25-(OH)2D3 and 24R,25-(OH)2D3.
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Nongenomic regulation of protein kinase C isoforms by the vitamin D metabolites 1 alpha,25-(OH)2D3 and 24R,25-(OH)2D3.

机译：Nongenomic调节蛋白激酶C亚型维生素D代谢产物1α,25 - (OH) 2 d3和24 r, 25 - (OH) 2 d3。

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摘要

Prior studies have shown that vitamin D regulation of protein kinase C activity (PKC) in the cell layer of chondrocyte cultures is cell maturation-dependent. In the present study, we examined the membrane distribution of PKC and whether 1 alpha,25-(OH)2D3 and 24R,25-(OH)2D3 can directly regulate enzyme activity in isolated plasma membranes and extracellular matrix vesicles. Matrix vesicle PKC was activated by bryostatin-1 and inhibited by a PKC-specific pseudosubstrate inhibitor peptide. Depletion of membrane PKC activity using isoform-specific anti-PKC antibodies suggested that PKC alpha is the major isoform in cell layer lysates as well as in plasma membranes isolated from both cell types; PKC zeta is the predominant form in matrix vesicles. This was confirmed in Western blots of immunoprecipitates as well as in studies using control peptides to block binding of the isoform specific antibody to the enzyme and using a PKC zeta-specific pseudosubstrate inhibitor peptide. The presence of PKC zeta in matrix vesicles was further verified by immunoelectron microscopy. Enzyme activity in the matrix vesicle was insensitive to exogenous lipid, whereas that in the plasma membrane required lipid for full activity. 1,25-(OH)2D3 and 24,25-(OH)2D3 inhibited matrix vesicle PKC, but stimulated plasma membrane PKC when added directly to the isolated membrane fractions. PKC activity in the matrix vesicle was calcium-independent, whereas that in the plasma membrane required calcium. Moreover, the vitamin D-sensitive PKC in matrix vesicles was not dependent on calcium, whereas the vitamin D-sensitive enzyme in plasma membranes was calcium-dependent. It is concluded that PKC isoforms are differentially distributed between matrix vesicles and plasma membranes and that enzyme activity is regulated in a membrane-specific manner. This suggests the existence of a nongenomic mechanism whereby the effects of 1,25-(OH)2D3 and 24,25-(OH)2D3 may be mediated via PKC. Further, PKC zeta may be important in nongenomic, autocrine signaltransduction at sites distal from the cell.
机译：之前的研究表明,维生素D的监管蛋白激酶C (PKC)活性的细胞层软骨细胞培养的细胞maturation-dependent。研究细胞膜PKC和分布是否1α,25 (OH) 2 d3和24 r, 25 - (OH) 2 d3直接调节酶活性在孤立等离子体膜和细胞外基质囊泡。PKC-specific bryostatin-1和抑制pseudosubstrate抑制肽。使用isoform-specific细胞膜PKC活性anti-PKC抗体建议PKCα在细胞层主要对碘氧基苯甲醚溶菌产物在等离子体膜分离细胞类型;囊泡。免疫沉淀反应,以及在研究中使用控制多肽阻止同种型的绑定特定的抗体酶和使用PKCzeta-specific pseudosubstrate抑制肽。基质小泡的PKCζ进一步验证了immunoelectron显微镜。酶活性的矩阵泡对外源性脂质,而在完整的所需的质膜脂质活动。抑制矩阵泡PKC,但刺激当直接添加到质膜PKC隔离膜分数。矩阵泡是calcium-independent,而在质膜所需的钙。此外,维生素D-sensitive PKC在矩阵囊泡是不依赖于钙,而在血浆维生素D-sensitive酶膜是calcium-dependent。PKC不同分布基质小泡和等离子体膜之间酶活动的监管membrane-specific方式。存在nongenomic机制的影响1,25 (OH) 2 d3, 24日,25 - (OH) 2 d3通过PKC介导的。重要的在nongenomic,自分泌signaltransduction网站远从细胞。

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