Ceramide-induced enhancement of secretory phospholipase A(2) expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells

Kitatani K; Akiba S; Sato T

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Ceramide-induced enhancement of secretory phospholipase A(2) expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells

机译：神经酰胺诱导增强的分泌性磷脂酶A（2）表达通过肿瘤坏死因子-α刺激的系膜细胞中活性氧的产生

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Since prostanoids such as prostaglandin E-2 play a pivotal role in modulating renal function, we investigated the involvement of ceramide in expression of secretory phospholipase A(2) (sPLA(2)) and cyclooxygenase-2 (COX-2) in tumor necrosis factor-alpha (TNF-alpha)-stimulated mesangial cells. TNF-alpha stimulation increased ceramide generation in parallel with a decrease in sphingomyelin. Pretreatment with exogenous sphingomyelinase (SMase) dose-dependently enhanced TNF-alpha-stimulated increases in COX-2 protein and sPLA(2) activity. SMase also augmented TNF-alpha-mediated nuclear factor kappaB (NF-kappaB) activation. N-acetylcysteine (NAC), an antioxidant, completely inhibited the SMase-induced increase in sPLA(2) activity, whereas NAC inhibited partially the activity stimulated with TNF-alpha alone. Under the conditions, NAC completely inhibited reactive oxygen species (ROS) production induced by SMase followed by TNF-alpha. These results suggest that ceramide elicits up-regulation of NF-kappaB through ROS production, which, in turn, leads to stimulation of COX-2 and sPLA(2) expression. Therefore, ceramide may be implicated in the pathogenesis of renal abnormalities. (C) 2004 Elsevier Inc. All rights reserved.

机译：由于前列腺素如前列腺素E-2在调节肾功能中起关键作用，因此我们调查了神经酰胺在肿瘤坏死中参与分泌性磷脂酶A（2）（sPLA（2））和环氧合酶2（COX-2）的表达因子-α（TNF-α）刺激的系膜细胞。 TNF-α刺激增加神经酰胺的产生，同时鞘磷脂减少。用外源鞘磷脂酶（SMase）进行剂量依赖性增强的TNF-α刺激的COX-2蛋白和sPLA（2）活性的增加。 SMase还增强了TNF-α介导的核因子kappaB（NF-kappaB）的激活。 N-乙酰半胱氨酸（NAC），一种抗氧化剂，完全抑制了SMase诱导的sPLA（2）活性的增加，而NAC部分抑制了单独用TNF-α刺激的活性。在这种条件下，NAC完全抑制了SMase和TNF-α诱导的活性氧（ROS）的产生。这些结果表明，神经酰胺通过ROS产生引起NF-κB的上调，进而导致刺激COX-2和sPLA（2）的表达。因此，神经酰胺可能与肾脏异常的发病机制有关。（C）2004 Elsevier Inc.保留所有权利。

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《Cellular Signalling》 |2004年第8期|共8页
作者
Kitatani K; Akiba S; Sato T;
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正文语种 eng
中图分类细胞形态学;
关键词
ceramide; secretory phospholipase A(2); cyclooxygenase-2; reactive oxygen species; nuclear factor kappa B; mesangial cells; tumor necrosis factor-alpha; KAPPA-B ACTIVATION; GROUP-II PHOSPHOLIPASE-A(2); ARACHIDONIC-ACID RELEASE; NITRIC-OXIDE SYNTHASE; PROSTAGLANDIN GENERATION; EPITHELIAL-CELLS; A(2) EXPRESSION; GENE-EXPRESSION; CYCLOOXYGENASE-2; KINASE;

机译：神经酰胺;分泌型磷脂酶A（2）;环氧合酶2;活性氧;核因子κB;系膜细胞;肿瘤坏死因子-α;KAPPA-B激活;GROUP-II磷脂酶-A（2）;花生四烯酸释放一氧化氮合酶;前列腺素生成;上皮细胞;A（2）表达;基因表达;环氧化酶-2;激酶;

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1. Ceramide-induced enhancement of secretory phospholipase A(2) expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells [J] . Kitatani K, Akiba S, Sato T Cellular Signalling . 2004,第8期

机译：神经酰胺诱导增强的分泌性磷脂酶A（2）表达通过肿瘤坏死因子-α刺激的系膜细胞中活性氧的产生
2. Inhibitory effect of butein on tumor necrosis factor-α-induced expression of cell adhesion molecules in human lung epithelial cells via inhibition of reactive oxygen species generation, NF-κB activation and Akt phosphorylation [J] . JangJ.H., YangE.S., MinK.-J., International journal of molecular medicine . 2012,第6期

机译：酪蛋白通过抑制活性氧的产生，NF-κB的活化和Akt的磷酸化对肿瘤坏死因子-α诱导的人肺上皮细胞粘附分子表达的抑制作用
3. Lactosylceramide‐Induced Phosphorylation Signaling to Group IVA Phospholipase A 2 2 via Reactive Oxygen Species in Tumor Necrosis Factor‐α‐Treated Cells [J] . Nakamura Hiroyuki, Moriyama Yuta, Watanabe Kazuaki, Journal of cellular biochemistry. . 2017,第12期

机译：乳糖基胺酰胺诱导的磷酸化信号传导至IVA磷脂酶A 2 2通过肿瘤坏死因子-α-处理的细胞中的反应性氧
4. Increased trans-endothelial cells permeability induced by oxidized lipoprotein(a) relates to reactive oxygen species generation and desmogleins expression [C] . Zuo Wang, Jian Yang, Xiao-lei Zhang, World Congress on Medical Physics and Biomedical Engineering . 2013

机译：氧化脂蛋白（a）诱导的跨内皮细胞通透性增加与活性氧的产生和桥粒糖蛋白的表达有关
5. Factors shed by breast tumor cells, tumor necrosis factor alpha converting enzyme activities, and the generation of pro-tumor macrophages. [D] . Rego, Stephen Lee. 2013

机译：乳腺肿瘤细胞脱落的因子，肿瘤坏死因子α转换酶的活性以及促肿瘤巨噬细胞的产生。
6. Activation and attenuation of transcription factor NF-kB in mouse glomerular mesangial cells in response to tumor necrosis factor-alpha immunoglobulin G and adenosine 3:5-cyclic monophosphate. Evidence for involvement of reactive oxygen species. [O] . J Satriano, D Schlondorff 1994

机译：小鼠肾小球系膜细胞中转录因子NF-kB的激活和减弱响应于肿瘤坏死因子-α免疫球蛋白G和腺苷3：5-环一磷酸。有活性氧参与的证据。
7. Ginkgo biloba Extract Inhibits Tumor Necrosis Factor-α–Induced Reactive Oxygen Species Generation, Transcription Factor Activation, and Cell Adhesion Molecule Expression in Human Aortic Endothelial Cells [O] . Jaw-Wen Chen, Yung-Hsiang Chen, Feng-Yan Lin, 2003

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8. IL-1 and Tumor Necrosis Factor-Alpha Each Up-Regulate Both the Expression of IFN-Gamma Receptors and Enhance IFN-Gamma-Induced HLA-DR Expression on Human Monocytes and a Human Monocytic Cell Line (THP-1) [R] . Krakauer, T., Oppenheim, J. J. 1993

机译：IL-1和肿瘤坏死因子-α各自上调IFN-γ受体的表达并增强人单核细胞和人单核细胞系（THp-1）上IFN-γ诱导的HLa-DR表达

Ceramide-induced enhancement of secretory phospholipase A(2) expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells

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