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4-羟基壬烯醛对血小板蛋白的修饰:抑制聚集和代谢的潜在机制

Modification of platelet proteins by 4-hydroxynonenal: Potential Mechanisms for inhibition of aggregation and metabolism.

作者信息

Ravi Saranya, Johnson Michelle S, Chacko Balu K, Kramer Philip A, Sawada Hirotaka, Locy Morgan L, Wilson Landon S, Barnes Stephen, Marques Marisa B, Darley-Usmar Victor M

机构信息

Department of Pathology; UAB Mitochondrial Medicine Laboratory; Center for Free Radical Biology.

The Targeted Metabolomics and Proteomics Laboratory.

出版信息

Free Radic Biol Med. 2016 Feb;91:143-53. doi: 10.1016/j.freeradbiomed.2015.10.408. Epub 2015 Oct 22.

Abstract

Platelet aggregation is an essential response to tissue injury and is associated with activation of pro-oxidant enzymes, such as cyclooxygenase, and is also a highly energetic process. The two central energetic pathways in the cell, glycolysis and mitochondrial oxidative phosphorylation, are susceptible to damage by reactive lipid species. Interestingly, how platelet metabolism is affected by the oxidative stress associated with aggregation is largely unexplored. To address this issue, we examined the response of human platelets to 4-hydroxynonenal (4-HNE), a reactive lipid species which is generated during thrombus formation and during oxidative stress. Elevated plasma 4-HNE has been associated with renal failure, septic shock and cardiopulmonary bypass surgery. In this study, we found that 4-HNE decreased thrombin stimulated platelet aggregation by approximately 60%. The metabolomics analysis demonstrated that underlying our previous observation of a stimulation of platelet energetics by thrombin glycolysis and TCA (Tricarboxylic acid) metabolites were increased. Next, we assessed the effect of both 4-HNE and alkyne HNE (A-HNE) on bioenergetics and targeted metabolomics, and found a stimulatory effect on glycolysis, associated with inhibition of bioenergetic parameters. In the presence of HNE and thrombin glycolysis was further stimulated but the levels of the TCA metabolites were markedly suppressed. Identification of proteins modified by A-HNE followed by click chemistry and mass spectrometry revealed essential targets in platelet activation including proteins involved in metabolism, adhesion, cytoskeletal reorganization, aggregation, vesicular transport, protein folding, antioxidant proteins, and small GTPases. In summary, the biological effects of 4-HNE can be more effectively explained in platelets by the integrated effects of the modification of an electrophile responsive proteome rather than the isolated effects of candidate proteins.

摘要

血小板聚集是对组织损伤的一种重要反应,与促氧化酶(如环氧化酶)的激活相关,并且也是一个高耗能过程。细胞中的两条核心能量途径,即糖酵解和线粒体氧化磷酸化,易受活性脂质物质的损害。有趣的是,血小板代谢如何受到与聚集相关的氧化应激影响在很大程度上尚未得到探索。为了解决这个问题,我们研究了人血小板对4-羟基壬烯醛(4-HNE)的反应,4-HNE是一种在血栓形成和氧化应激过程中产生的活性脂质物质。血浆4-HNE升高与肾衰竭、脓毒症休克和体外循环手术有关。在本研究中,我们发现4-HNE使凝血酶刺激的血小板聚集降低了约60%。代谢组学分析表明,在我们之前观察到的凝血酶通过糖酵解刺激血小板能量代谢的基础上,三羧酸(TCA)代谢产物增加。接下来,我们评估了4-HNE和炔基HNE(A-HNE)对生物能量学和靶向代谢组学的影响,发现对糖酵解有刺激作用,同时伴随着生物能量学参数的抑制。在HNE和凝血酶存在的情况下,糖酵解进一步受到刺激,但TCA代谢产物的水平明显受到抑制。通过点击化学和质谱鉴定A-HNE修饰的蛋白质,揭示了血小板激活中的关键靶点,包括参与代谢、黏附、细胞骨架重组、聚集、囊泡运输、蛋白质折叠、抗氧化蛋白和小GTP酶的蛋白质。总之,4-HNE在血小板中的生物学效应可以通过亲电反应蛋白质组修饰的综合效应而不是候选蛋白质的单独效应来更有效地解释。

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引用本文的文献

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1
Metabolic plasticity in resting and thrombin activated platelets.静息和凝血酶激活血小板中的代谢可塑性。
PLoS One. 2015 Apr 13;10(4):e0123597. doi: 10.1371/journal.pone.0123597. eCollection 2015.

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