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首页> 外文期刊>Journal of applied toxicology >Arsenic inhibits mast cell degranulation via suppression of early tyrosine phosphorylation events
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Arsenic inhibits mast cell degranulation via suppression of early tyrosine phosphorylation events

机译：砷通过抑制早期酪氨酸磷酸化事件抑制肥大细胞脱粒

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Exposure to arsenic is a global health concern. We previously documented an inhibitory effect of inorganic Arsenite on IgE-mediated degranulation of RBL-2H3 mast cells (Hutchinson et al., 2011; J. Appl. Toxicol. 31: 231-241). Mast cells are tissue-resident cells that are positioned at the host-environment interface, thereby serving vital roles in many physiological processes and disease states, in addition to their well-known roles in allergy and asthma. Upon activation, mast cells secrete several mediators from cytoplasmic granules, in degranulation. The present study is an investigation of Arsenite's molecular target(s) in the degranulation pathway. Here, we report that arsenic does not affect degranulation stimulated by either the Ca2+ ionophore A23187 or thapsigargin, which both bypass early signaling events. Arsenic also does not alter degranulation initiated by another non-IgE-mediated mast cell stimulant, the G-protein activator compound 48/80. However, arsenic inhibits Ca2+ influx into antigen-activated mast cells. These results indicate that the target of arsenic in the degranulation pathway is upstream of the Ca2+ influx. Phospho-Syk and phospho-p85 phosphoinositide 3-kinase enzyme-linked immunosorbent assays data show that arsenic inhibits early phosphorylation events. Taken together, this evidence indicates that the mechanism underlying arsenic inhibition of mast cell degranulation occurs at the early tyrosine phosphorylation steps in the degranulation pathway. Copyright (c) 2016 John Wiley & Sons, Ltd.
机译：砷暴露是全球健康问题。我们先前已记录了无机亚砷酸盐对IgE介导的RBL-2H3肥大细胞脱颗粒的抑制作用（Hutchinson等人，2011; J。Appl。Toxicol。31：231-241）。肥大细胞是位于宿主-环境界面处的组织驻留细胞，因此除了在变态反应和哮喘中的众所周知的作用外，在许多生理过程和疾病状态中也起着至关重要的作用。激活后，肥大细胞在脱粒过程中从细胞质颗粒分泌几种介体。本研究是对脱颗粒途径中砷分子目标的研究。在这里，我们报告说砷不影响由Ca2 +离子载体A23187或毒胡萝卜素刺激的脱粒，这两者都绕过了早期信号事件。砷也不会改变由另一种非IgE介导的肥大细胞刺激剂G蛋白激活剂化合物48/80引发的脱粒。但是，砷会抑制Ca2 +流入抗原激活的肥大细胞。这些结果表明，脱粒途径中的砷靶位于Ca2 +流入量的上游。 Phospho-Syk和phospho-p85磷酸肌醇3-激酶酶联免疫吸附试验数据表明，砷可抑制早期的磷酸化作用。综上所述，该证据表明砷抑制肥大细胞脱粒的潜在机理发生在脱粒途径中的酪氨酸磷酸化早期阶段。版权所有（c）2016 John Wiley＆Sons，Ltd.

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