暴露于香烟烟雾中的T淋巴细胞释放的微粒有助于肺微血管内皮细胞的自噬和凋亡功能障碍

IF 3.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Gang Chen , Zhaoji Meng , Pei Wang
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引用次数: 0

摘要

吸烟可引起血管内皮功能障碍;然而,其潜在机制尚未完全阐明。我们假设T淋巴细胞衍生微粒(TLMPs)参与香烟相关疾病,特别是那些涉及血管内皮的疾病。研究了香烟烟雾对人淋巴细胞微颗粒释放的影响。研究人员还测量了香烟烟雾诱导的TLMPs对内皮细胞增殖/凋亡、自噬和细胞因子水平的影响。值得注意的是,我们进一步研究了内皮细胞自噬和凋亡功能障碍的潜在机制。香烟烟雾促进了T淋巴细胞微粒的释放。特别是当T淋巴细胞预先暴露于香烟烟雾中时,TLMPs减弱内皮细胞增殖,但促进内皮细胞凋亡/自噬和促炎细胞因子的表达。其潜在机制可能涉及氧化应激和STAT3磷酸化紊乱。综上所述,暴露于香烟烟雾中的T淋巴细胞释放的微粒有助于肺微血管内皮细胞的自噬和凋亡功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cigarette smoke-exposed microparticles released from T lymphocytes contribute to autophagy and apoptosis dysfunction in pulmonary microvascular endothelial cells
Cigarette smoke can cause dysfunction of the vascular endothelium; however, the underlying mechanisms have not been fully elucidated. We hypothesized that T lymphocyte-derived microparticles (TLMPs) are involved in cigarette-related diseases, especially those involving the vascular endothelium. The effect of cigarette smoke on the release of microparticles from human lymphocytes was investigated. The contributions of TLMPs induced by cigarette smoke to endothelial proliferation/apoptosis, autophagy and cytokine levels were also measured. Notably, the potential mechanism of autophagy and apoptosis dysfunction in endothelial cells was further examined. Cigarette smoke promoted the release of microparticles from T lymphocytes. TLMPs attenuated endothelial proliferation but promoted endothelial apoptosis/autophagy and the expression of proinflammatory cytokines, especially when T lymphocytes were preexposed to cigarette smoke. The potential mechanism may involve disorders of oxidative stress and STAT3 phosphorylation. In conclusion, cigarette smoke-exposed microparticles released from T lymphocytes contribute to autophagy and apoptosis dysfunction in pulmonary microvascular endothelial cells.
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来源期刊
Molecular immunology
Molecular immunology 医学-免疫学
CiteScore
6.90
自引率
2.80%
发文量
324
审稿时长
50 days
期刊介绍: Molecular Immunology publishes original articles, reviews and commentaries on all areas of immunology, with a particular focus on description of cellular, biochemical or genetic mechanisms underlying immunological phenomena. Studies on all model organisms, from invertebrates to humans, are suitable. Examples include, but are not restricted to: Infection, autoimmunity, transplantation, immunodeficiencies, inflammation and tumor immunology Mechanisms of induction, regulation and termination of innate and adaptive immunity Intercellular communication, cooperation and regulation Intracellular mechanisms of immunity (endocytosis, protein trafficking, pathogen recognition, antigen presentation, etc) Mechanisms of action of the cells and molecules of the immune system Structural analysis Development of the immune system Comparative immunology and evolution of the immune system "Omics" studies and bioinformatics Vaccines, biotechnology and therapeutic manipulation of the immune system (therapeutic antibodies, cytokines, cellular therapies, etc) Technical developments.
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