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酰基链依赖性溶血磷脂酰胆碱对内皮细胞中环氧化酶（COX）-2 表达的影响。

Acyl chain-dependent effect of lysophosphatidylcholine on cyclooxygenase (COX)-2 expression in endothelial cells.

机构信息

Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Harrachgasse 21/III, Medical University Graz, 8010 Graz, Austria.

出版信息

Atherosclerosis. 2012 Oct;224(2):348-54. doi: 10.1016/j.atherosclerosis.2012.07.038. Epub 2012 Aug 2.

DOI:10.1016/j.atherosclerosis.2012.07.038
PMID:22901457
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3465554/
Abstract

OBJECTIVE

Previously we identified palmitoyl-, oleoyl- linoleoyl-, and arachidonoyl-lysophosph-atidylcholine (LPC 16:0, 18:1, 18:2 and 20:4) as the most prominent LPC species generated by endothelial lipase (EL). In the present study, we examined the capacity of those LPC to modulate expression of cyclooxygenase (COX)-2 in vascular endothelial cells.

METHODS & RESULTS: LPC 16:0 and 20:4 promoted both COX-2 mRNA- and protein synthesis with different potencies and kinetics. While LPC 18:1 induced a weak and transient increase in COX-2 mRNA, but not protein, LPC 18:2 increased COX-2 protein, without impacting mRNA. Chelation of intracellular Ca(2+) and inhibition of p38 MAPK markedly attenuated 16:0 LPC- and 20:4 LPC- elicited induction of COX-2 expression, whereas inhibition of phospholipase C (PLC) attenuated only the effect of 16:0 LPC. LPC 16:0 and 20:4 differed markedly in their potencies to increase cytosolic Ca(2+) concentration and in the kinetics of p38 MAPK activation. While the effects of 16:0 and 20:4 LPC on COX-2 expression were profoundly sensitive to silencing of either c-Jun or p65 (NF-κB), respectively, silencing of cyclic AMP responsive element binding protein (CREB) attenuated markedly the effect of both LPC.

CONCLUSION

Our results indicate that the tested LPC species are capable of inducing COX-2 expression, whereby the efficacy and the relative contribution of underlying signaling mechanisms markedly differ, due to the length and degree of saturation of LPC acyl chains.

摘要

目的

先前我们鉴定出棕榈酰、油酰、亚油酰和花生四烯酰溶血磷脂酰胆碱（LPC 16:0、18:1、18:2 和 20:4）是内皮脂肪酶（EL）生成的最主要的溶血磷脂酰胆碱（LPC）种类。在本研究中，我们检测了这些 LPC 调节血管内皮细胞中环氧化酶（COX）-2 表达的能力。

方法和结果

LPC 16:0 和 20:4 以不同的效力和动力学促进 COX-2 mRNA 和蛋白质合成。虽然 LPC 18:1 诱导 COX-2 mRNA 产生微弱而短暂的增加，但不增加蛋白质，LPC 18:2 增加 COX-2 蛋白质，而不影响 mRNA。细胞内 Ca2+螯合和 p38 MAPK 抑制显著减弱 16:0 LPC 和 20:4 LPC 引起的 COX-2 表达诱导，而 PLC 抑制仅减弱 16:0 LPC 的作用。LPC 16:0 和 20:4 在增加细胞质 Ca2+浓度的效力和 p38 MAPK 激活的动力学方面有显著差异。虽然 16:0 和 20:4 LPC 对 COX-2 表达的影响对 c-Jun 或 p65（NF-κB）的沉默分别非常敏感，但环磷酸腺苷反应元件结合蛋白（CREB）的沉默显著减弱了两种 LPC 的作用。

结论

我们的结果表明，所测试的 LPC 种类能够诱导 COX-2 表达，由于 LPC 酰基链的长度和饱和度的不同，其效力和潜在信号机制的相对贡献显著不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/57721bad7f3d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/3c69d36e6f92/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/93b96b75a3bf/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/8a1e0c9efc1c/figs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/4c9018734ca5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/41466904bcd3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/990c2344f7e0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/57721bad7f3d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/3c69d36e6f92/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/93b96b75a3bf/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/8a1e0c9efc1c/figs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/4c9018734ca5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/41466904bcd3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/990c2344f7e0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/636d/3465554/57721bad7f3d/gr4.jpg

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