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Journal of lipid mediators最新文献

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PGE2 in the perinatal brain: local synthesis and transfer across the blood brain barrier. 围产期脑中的PGE2:局部合成并通过血脑屏障转移。
Pub Date : 1993-03-01
S A Jones, S L Adamson, D Engelberts, I Bishai, J Norton, F Coceani
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引用次数: 0
Expression of 5-lipoxygenase and biosynthesis of leukotriene B4 in human monomorphonuclear leukocytes. 5-脂氧合酶在人单核白细胞中的表达及白三烯B4的生物合成。
Pub Date : 1993-03-01
H E Claesson, P J Jakobsson, D Steinhilber, B Odlander, B Samuelsson
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引用次数: 0
Differential regulation of cytokine and cytokine receptor genes by PAF, LTB4 and PGE2. PAF、LTB4和PGE2对细胞因子和细胞因子受体基因的差异调控。
Pub Date : 1993-03-01
M Rola-Pleszczynski, M Thivierge, N Gagnon, C Lacasse, J Stankova

Immune and inflammatory responses involve a whole array of cells and cell products which interact and mutually regulate each other. Many of these interactions are mediated by cytokines acting through specific receptors. Furthermore, lipid mediators such as PAF and the arachidonic acid metabolites LTB4 and PGE2 are known to affect several of the mechanisms involved in the regulation of the immune and inflammatory responses. In this paper, we review recent data from our laboratory illustrating the differential regulation of IL-6 and TNF alpha production and IL-2 receptor alpha and beta expression by these lipid mediators. We show that the regulation of these genes is both transcriptional and post-transcriptional, and that LT and PG can also be involved as second messengers in these regulatory processes.

免疫和炎症反应涉及一系列细胞和细胞产物,它们相互作用并相互调节。许多这些相互作用是由细胞因子通过特定受体介导的。此外,已知脂质介质如PAF和花生四烯酸代谢物LTB4和PGE2可影响参与免疫和炎症反应调节的几种机制。在本文中,我们回顾了我们实验室最近的数据,说明了这些脂质介质对IL-6和TNF α产生以及IL-2受体α和β表达的差异调节。我们发现这些基因的调控是转录和转录后的,并且LT和PG也可以作为第二信使参与这些调控过程。
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引用次数: 0
Prostaglandins as modulators rather than mediators of inflammation. 前列腺素是炎症的调节剂而不是介质。
Pub Date : 1993-03-01
G Weissmann
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引用次数: 0
Enhancement by GM-CSF of agonist-induced 5-lipoxygenase activation in human neutrophils involves protein synthesis and gene transcription. GM-CSF增强激动剂诱导的人中性粒细胞5-脂氧合酶激活涉及蛋白质合成和基因转录。
Pub Date : 1993-03-01
P P McDonald, M Pouliot, P Borgeat

We investigated the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the 5-lipoxygenase (5-LO) component of the leukotriene (LT) biosynthetic pathway of human neutrophils, in order to better understand the mechanism whereby the cytokine primes for LT synthesis. We found that GM-CSF increased 5-LO activation elicited by platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (fMLP), C5a, LTB4, IL-8 and calcium ionophore A23187, as determined by using an exogenous substrate. A close correlation was observed between the priming kinetics of GM-CSF on 5-LO activation and on LT synthesis; moreover, the effects of the cytokine on both 5-LO activation and LT synthesis were inhibited when the cells had been exposed to either the protein synthesis inhibitor, cycloheximide (CX), or the transcription inhibitor, actinomycin D (AD), prior to incubation with GM-CSF. These results raise the possibility that the priming by GM-CSF of LT synthesis may involve an effect of the cytokine on 5-LO protein synthesis and gene expression.

我们研究了粒细胞-巨噬细胞集落刺激因子(GM-CSF)对人中性粒细胞白三烯(LT)生物合成途径中5-脂氧合酶(5-LO)组分的影响,以便更好地了解细胞因子启动LT合成的机制。我们发现GM-CSF增加了血小板活化因子(PAF)、n -甲酰基-甲硫基-亮基-苯丙氨酸(fMLP)、C5a、LTB4、IL-8和钙离子载体A23187所引起的5-LO活化。GM-CSF对5-LO活化和LT合成的启动动力学密切相关;此外,当细胞在GM-CSF孵育前暴露于蛋白质合成抑制剂环己亚胺(CX)或转录抑制剂放线菌素D (AD)时,细胞因子对5-LO活化和LT合成的影响均被抑制。这些结果提出了GM-CSF引发LT合成的可能性,可能涉及细胞因子对5-LO蛋白合成和基因表达的影响。
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引用次数: 0
Leukotriene A4 hydrolase: structural and functional properties of the active center. 白三烯A4水解酶:活性中心的结构和功能性质。
Pub Date : 1993-03-01
J Z Haeggström, A Wetterholm, J F Medina, B Samuelsson

Leukotriene (LT) A4 hydrolase (EC 3.3.2.6) is a bifunctional zinc metalloenzyme that possesses both an epoxide hydrolase activity, i.e., the well-known conversion of LTA4 into the proinflammatory substance LTB4, and a recently discovered peptidase activity. We have employed biochemical/kinetic analyses of native enzyme as well as site directed mutagenesis towards a recombinant enzyme to explore structural and functional properties of the enzyme active center. Thus, we have found that the peptidase activity is selectively stimulated by chloride ions, in a manner that suggests the presence of an anion binding site. Furthermore, a number of mutated enzymes have been constructed, expressed in E. coli, and purified to homogeneity to allow enzyme activity determinations and zinc analyses. The catalytic properties and zinc contents of these mutated enzymes establish the three zinc binding ligands of the protein and identify Glu-296 as a catalytic amino acid, directly involved in the peptidase, but not in the epoxide hydrolase reaction. In conclusion, our data provide strong evidence that the two catalytic activities of LTA4 hydrolase are exerted via non-identical but overlapping active sites.

白三烯(LT) A4水解酶(EC 3.3.2.6)是一种双功能锌金属酶,具有环氧化物水解酶活性,即众所周知的将LTA4转化为促炎物质LTB4,以及最近发现的肽酶活性。我们利用天然酶的生化/动力学分析以及对重组酶的定点诱变来探索酶活性中心的结构和功能特性。因此,我们发现肽酶活性被氯离子选择性地刺激,以一种表明阴离子结合位点存在的方式。此外,已经构建了一些突变酶,在大肠杆菌中表达,并纯化到同质性,以便进行酶活性测定和锌分析。这些突变酶的催化性质和锌含量确定了蛋白的三个锌结合配体,并确定了Glu-296是一个催化氨基酸,直接参与肽酶反应,但不参与环氧化物水解酶反应。总之,我们的数据提供了强有力的证据,证明LTA4水解酶的两种催化活性是通过不相同但重叠的活性位点发挥的。
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引用次数: 0
Biochemical and molecular biological approaches to two types of arachidonate 12-lipoxygenase. 两类花生四烯酸12-脂加氧酶的生化和分子生物学研究。
Pub Date : 1993-03-01
S Yamamoto, T Yoshimoto, Y Takahashi, H Suzuki, T Arakawa, K Kishimoto, T Hada, T Oshima, J Murakami, Y Yamamoto
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引用次数: 0
Human 15-lipoxygenase: induction by interleukin-4 and insights into positional specificity. 人15-脂氧合酶:由白细胞介素-4诱导和位置特异性的见解。
Pub Date : 1993-03-01
E Sigal, D L Sloane, D J Conrad

Arachidonate 15-lipoxygenase (15-lipoxygenase) is a lipid-peroxidizing enzyme associated with specific inflammatory cells seen in asthma and atherosclerosis. In atherosclerosis, 15-lipoxygenase is induced in the macrophages of human and rabbit lesions and has been implicated in foam cell formation. In human lung, 15-lipoxygenase is preferentially expressed in airway epithelial cells and eosinophils. Our studies have focused both on the regulation of expression and on the structure-function relationships of the enzyme. To determine factors that could regulate expression, peripheral blood monocytes were purified and cultured with combinations of 18 factors. Only interleukin-4 (60 pM) induced 15-lipoxygenase mRNA, protein and enzymatic activity. Interferon-gamma (100 pM) inhibited the interleukin-4 dependent induction of 15-lipoxygenase. Results with cultured human airway cells were similar. These data suggest that expression of 15-lipoxygenase is regulated by interleukin-4, and that 15-lipoxygenase is a potential downstream effector molecule for this potent cytokine. In parallel studies, we have investigated determinants of positional specificity using site-directed mutagenesis and bacterial expression of human 15-lipoxygenase. Hypotheses for mutagenesis were derived from an analysis of conserved differences among multiple lipoxygenase sequences. Switching four amino acids in 15-lipoxygenase to their counterparts in 12-lipoxygenase resulted in a variant enzyme that produced equal 12- and 15-lipoxygenation. Further analysis has identified two amino acids that completely control the positional specificity of 15-lipoxygenase. These data have led to a preliminary model of the enzyme's active site region.

花生四烯酸15-脂氧合酶(15-脂氧合酶)是一种与哮喘和动脉粥样硬化中特定炎症细胞相关的脂质过氧化酶。在动脉粥样硬化中,15-脂氧合酶在人和兔病变的巨噬细胞中被诱导,并与泡沫细胞的形成有关。在人肺中,15-脂氧合酶优先在气道上皮细胞和嗜酸性粒细胞中表达。我们的研究主要集中在表达调控和酶的结构-功能关系。为了确定调节表达的因子,我们纯化外周血单核细胞,并将18种因子联合培养。只有白细胞介素-4 (60 pM)能诱导15-脂氧合酶mRNA、蛋白和酶活性。干扰素- γ (100 pM)抑制白细胞介素-4依赖性诱导15-脂氧合酶。与培养的人气道细胞结果相似。这些数据表明15-脂氧合酶的表达受白细胞介素-4的调控,15-脂氧合酶是这种强效细胞因子的潜在下游效应分子。在平行研究中,我们已经研究了位置特异性的决定因素,使用定点诱变和人类15-脂氧合酶的细菌表达。突变的假设来源于对多个脂氧合酶序列之间保守差异的分析。将15-脂氧合酶中的四个氨基酸与12-脂氧合酶中的对应氨基酸交换,产生了一种变体酶,可以产生相等的12-脂氧合和15-脂氧合。进一步的分析已经确定了两个氨基酸完全控制15-脂氧合酶的位置特异性。这些数据导致了酶活性位点区域的初步模型。
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引用次数: 0
Interleukin 1 and interleukin 6 inhibition of mesangial cell proliferation: role of PGE2. 白细胞介素1和白细胞介素6抑制系膜细胞增殖:PGE2的作用。
Pub Date : 1993-03-01
D G Matsell, L W Gaber, E Sehic, K U Malik
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引用次数: 0
Effect of aging on renal cytochrome P450-dependent arachidonic acid metabolism in Dahl rats. 衰老对Dahl大鼠肾细胞色素p450依赖性花生四烯酸代谢的影响。
Pub Date : 1993-03-01
K Omata, E Tsutsumi, H L Sheu, Y Utsumi, K Abe

We investigated the age-related changes of renal cytochrome P450-dependent arachidonic acid metabolism in 3-, 5-, 7-, 9-, 11-, 13- and 20-week-old male Dahl salt-sensitive (DS) and -resistant (DR) rats on a low sodium diet (0.3% NaCl). NADPH-dependent arachidonic acid metabolism was separated and measured by a radio-HPLC system. The formation of 19-hydroxyeicosatetraenoic acid (HETE), 20 HETE, 1,20-dioic acid, epoxyeicosatrienoic acids (EETs), and dihydroxyeicosatrienoic acid (DHET) was age dependent in both DS and DR rats. omega-Hydroxylase (20-HETE and 1,20-dioic acid formation) and (omega-1)-hydroxylase (19-HETE formation) were increased from 3 to 5 weeks age, then decreased with aging in DR rats. Whilst omega/(omega-1)-hydroxylase activities were increased from 3- to 9-week-old rats, they decreased with aging in DS rats. omega/(omega-1)-Hydroxylase activities were higher in 3-5-week-old DR than DS rats. Epoxygenase activities (EETs and DHET formations) were highest in 3-week-old DS and DR rats, and showed no significant differences between two strains of rats at any ages tested. Renal cytochrome P450-dependent arachidonic acid metabolites have a wide and contrasting spectrum of biological and renal effects, and their relative rates of production may influence not only renal hemodynamics but also pro- and antihypertensive mechanisms of hypertension in Dahl rats.

我们研究了低钠饮食(0.3% NaCl)下3、5、7、9、11、13和20周龄雄性Dahl盐敏感(DS)和耐盐(DR)大鼠肾脏细胞色素p450依赖性花生四烯酸代谢的年龄相关变化。采用放射性高效液相色谱法分离并测定了nadph依赖性花生四烯酸代谢。在DS和DR大鼠中,19-羟基二十碳四烯酸(HETE)、20- HETE、1,20-二酸、环氧二十碳三烯酸(EETs)和二羟基二十碳三烯酸(DHET)的形成与年龄有关。DR大鼠3 ~ 5周龄ω -羟化酶(20-HETE和1,20-二酸生成)和(ω -1)-羟化酶(19-HETE生成)升高,随后随年龄增长而降低。虽然omega/(omega-1)-羟化酶活性在3周龄至9周龄的大鼠中有所增加,但在DS大鼠中随着年龄的增长而下降。3-5周龄DR的omega/(omega-1)-羟化酶活性高于DS大鼠。环氧合酶活性(EETs和DHET形成)在3周龄DS和DR大鼠中最高,在任何年龄两品系大鼠之间均无显著差异。肾细胞色素p450依赖性花生四烯酸代谢物具有广泛而不同的生物学和肾脏效应,其相对产生率可能不仅影响肾脏血流动力学,还影响达尔大鼠高血压的促高血压和抗高血压机制。
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Journal of lipid mediators
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