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ATP 消耗与渗出中性粒细胞的胞吞作用偶联。

ATP Consumption Is Coupled with Endocytosis in Exudated Neutrophils.

机构信息

Department of Radiobiology and Hygiene Management, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.

The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.

出版信息

Int J Mol Sci. 2023 May 20;24(10):9039. doi: 10.3390/ijms24109039.

DOI:10.3390/ijms24109039
PMID:37240384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10219472/
Abstract

Neutrophil energy metabolism during phagocytosis has been previously reported, and adenosine triphosphate (ATP) plays a crucial role in endocytosis. Neutrophils are prepared by intraperitoneal injection of thioglycolate for 4 h. We previously reported a system established for measuring particulate matter endocytosis by neutrophils using flow cytometry. In this study, we utilized this system to investigate the relationship between endocytosis and energy consumption in neutrophils. A dynamin inhibitor suppressed ATP consumption triggered by neutrophil endocytosis. In the presence of exogenous ATP, neutrophils behave differently during endocytosis depending on ATP concentration. The inhibition of ATP synthase and nicotinamide adenine dinucleotide phosphate oxidase but not phosphatidylinositol-3 kinase suppresses neutrophil endocytosis. The nuclear factor kappa B was activated during endocytosis and inhibited by I kappa B kinase (IKK) inhibitors. Notably, IKK inhibitors restored endocytosis-triggered ATP consumption. Furthermore, data from the NLR family pyrin domain containing three knockout mice suggest that inflammasome activation is not involved in neutrophil endocytosis or concomitant ATP consumption. To summarize, these molecular events occur via endocytosis, which is closely related to ATP-centered energy metabolism.

摘要

中性粒细胞吞噬作用过程中的能量代谢此前已有报道,三磷酸腺苷(ATP)在胞吞作用中起着至关重要的作用。通过腹腔注射巯基乙醇 4 小时来制备中性粒细胞。我们之前报道了一种使用流式细胞术测量中性粒细胞吞噬颗粒物质的系统。在本研究中,我们利用该系统研究了中性粒细胞内吞作用与能量消耗之间的关系。使用一种动力蛋白抑制剂抑制了中性粒细胞胞吞作用引发的 ATP 消耗。在存在外源性 ATP 的情况下,ATP 浓度会影响中性粒细胞的内吞作用方式。ATP 合酶和烟酰胺腺嘌呤二核苷酸磷酸氧化酶抑制剂而非磷脂酰肌醇-3 激酶抑制剂可抑制中性粒细胞的胞吞作用。核因子 kappa B 在胞吞作用过程中被激活,并被 I kappa B 激酶(IKK)抑制剂抑制。值得注意的是,IKK 抑制剂恢复了内吞作用触发的 ATP 消耗。此外,来自 NLR 家族含有三个吡喃结构域的蛋白 3 缺失小鼠的数据表明,NLRP3 炎性小体的激活不参与中性粒细胞的内吞作用或伴随的 ATP 消耗。综上所述,这些分子事件通过与 ATP 相关的能量代谢密切相关的内吞作用发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/729e2e5a1d88/ijms-24-09039-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/36b3a3a9340d/ijms-24-09039-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/19889730a690/ijms-24-09039-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/8d3d202054b7/ijms-24-09039-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/729e2e5a1d88/ijms-24-09039-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/36b3a3a9340d/ijms-24-09039-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/b12a761ff89e/ijms-24-09039-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/39c5162a54a3/ijms-24-09039-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/19889730a690/ijms-24-09039-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/8d3d202054b7/ijms-24-09039-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0079/10219472/729e2e5a1d88/ijms-24-09039-g007.jpg

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