蛋白质组学揭示了吸入有臭氧或无臭氧的环境颗粒物质后心脏炎症和代谢反应的差异。

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Toxicology Pub Date : 2024-12-01 Epub Date: 2024-10-14 DOI:10.1007/s12012-024-09931-9
Yue Ge, Maliha S Nash, Witold M Winnik, Maribel Bruno, William T Padgett, Rachel D Grindstaff, Mehdi S Hazari, Aimen K Farraj
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引用次数: 0

摘要

吸入环境颗粒物(PM)和臭氧(O3)与心血管发病率和死亡率的增加有关。然而,可吸入颗粒物和臭氧对心脏功能障碍和疾病的交互影响尚未得到深入研究,特别是在蛋白质组水平上。本研究的目的是识别和比较同时暴露于高浓度环境颗粒物和臭氧的自发性高血压(SH)大鼠的蛋白质组变化,重点研究炎症和代谢途径,这两种途径是与心功能障碍的病理生理学有关的主要途径。为此,我们使用多重酶联免疫吸附试验(ELISA)测量并比较了 9 种关键的促炎和抗炎细胞因子的表达状态变化,并使用二维电泳(2-DE)和质谱分析(MS)测量并比较了单独暴露于 CAPs、单独暴露于 O3 和 CAPs + O3 的 SH 大鼠心脏组织中涉及 ATP 生成、氧化磷酸化、细胞骨架组织和应激反应的 450 种代谢蛋白的表达状态变化。蛋白质组表达谱分析显示,单用 CAPs、单用 O3 和 CAPs + O3 可不同程度地改变蛋白质表达模式,并利用不同的机制影响炎症和代谢途径及反应。对蛋白质组数据进行的Ingenuity路径分析(IPA)表明,以间隙连接α-1蛋白(GJA 1)为中心的代谢蛋白网络与以核因子卡巴β(NF-kB)为中心的炎症细胞因子网络相互关联,这可能表明炎症诱导了代谢通路的改变,反之亦然,共同导致了CAPs和O3暴露下心脏功能障碍的发生。这些发现可能会加深人们对空气污染诱发心脏功能障碍的病理生理学的理解,并提供有关作用机制的可检验假设。
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Proteomics Reveals Divergent Cardiac Inflammatory and Metabolic Responses After Inhalation of Ambient Particulate Matter With or Without Ozone.

Inhalation of ambient particulate matter (PM) and ozone (O3) has been associated with increased cardiovascular morbidity and mortality. However, the interactive effects of PM and O3 on cardiac dysfunction and disease have not been thoroughly examined, especially at a proteomic level. The purpose of this study was to identify and compare proteome changes in spontaneously hypertensive (SH) rats co-exposed to concentrated ambient particulates (CAPs) and O3, with a focus on investigating inflammatory and metabolic pathways, which are the two major ones implicated in the pathophysiology of cardiac dysfunction. For this, we measured and compared changes in expression status of 9 critical pro- and anti-inflammatory cytokines using multiplexed ELISA and 450 metabolic proteins involved in ATP production, oxidative phosphorylation, cytoskeletal organization, and stress response using two-dimensional electrophoresis (2-DE) and mass spectrometry (MS) in cardiac tissue of SH rats exposed to CAPs alone, O3 alone, and CAPs + O3. Proteomic expression profiling revealed that CAPs alone, O3 alone, and CAPs + O3 differentially altered protein expression patterns, and utilized divergent mechanisms to affect inflammatory and metabolic pathways and responses. Ingenuity Pathway Analysis (IPA) of the proteomic data demonstrated that the metabolic protein network centered by gap junction alpha-1 protein (GJA 1) was interconnected with the inflammatory cytokine network centered by nuclear factor kappa beta (NF-kB) potentially suggesting inflammation-induced alterations in metabolic pathways, or vice versa, collectively contributing to the development of cardiac dysfunction in response to CAPs and O3 exposure. These findings may enhance understanding of the pathophysiology of cardiac dysfunction induced by air pollution and provide testable hypotheses regarding mechanisms of action.

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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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