输注血管紧张素 II 后,肿瘤坏死因子 alpha 可诱导下丘脑室旁核神经元产生 NOX2 依赖性活性氧。

IF 4.4 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Neurochemistry international Pub Date : 2024-08-02 DOI:10.1016/j.neuint.2024.105825
Clara Woods , Gang Wang , Teresa A. Milner , Michael J. Glass
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引用次数: 0

摘要

有证据表明,肿瘤坏死因子α(TNFα)会影响下丘脑室旁核(PVN)内协调的自律神经过程,然而,TNFα在这一脑区发挥作用的信号机制尚不清楚。在非神经元细胞类型中,TNFα已被证明在典型的NADPH氧化酶(NOX2)介导的活性氧(ROS)产生中发挥了重要作用,众所周知,活性氧分子也与高血压密切相关。然而,人们对 TNFα 在高血压背景下 PVN 中 NOX2 依赖性 ROS 生成中的作用知之甚少。我们利用双标记免疫电子显微镜和双氢乙锭显微荧光成像技术,提供了 TNFα 和 NOX2 在视网膜神经元中相互作用的结构和功能证据。TNFα 1型受体(TNFR1)是PVN中TNFα信号传导的主要介质,它与NOX2的催化gp91phox亚基共同定位在PVN神经元突触后部位。此外,在注射血管紧张素 II(AngII)十四天后,双标记树突轮廓有所增加。使用二氢乙啶(DHE)微荧光成像技术还显示,在向脊髓投射的离体PVN神经元中,TNFα的应用导致了依赖于NOX2的ROS增加。此外,输注 AngII 后,TNFα 介导的 ROS 生成增加。TNFR1和gp91phox定位为快速相互作用,尤其是在PVN-脊髓投射神经元中,这一发现提供了一个分子底物,炎症信号传导和氧化应激可能共同导致AngII高血压。
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Tumor necrosis factor alpha induces NOX2-dependent reactive oxygen species production in hypothalamic paraventricular nucleus neurons following angiotensin II infusion

There is evidence that tumor necrosis factor alpha (TNFα) influences autonomic processes coordinated within the hypothalamic paraventricular nucleus (PVN), however, the signaling mechanisms subserving TNFα′s actions in this brain area are unclear. In non-neuronal cell types, TNFα has been shown to play an important role in canonical NADPH oxidase (NOX2)-mediated production of reactive oxygen species (ROS), molecules also known to be critically involved in hypertension. However, little is known about the role of TNFα in NOX2-dependent ROS production in the PVN within the context of hypertension. Using dual labeling immunoelectron microscopy and dihydroethidium (DHE) microfluorography, we provide structural and functional evidence for interactions between TNFα and NOX2 in the PVN. The TNFα type 1 receptor (TNFR1), the major mediator of TNFα signaling in the PVN, was commonly co-localized with the catalytic gp91phox subunit of NOX2 in postsynaptic sites of PVN neurons. Additionally, there was an increase in dual labeled dendritic profiles following fourteen-day slow-pressor angiotensin II (AngII) infusion. Using DHE microfluorography, it was also shown that TNFα application resulted in a NOX2-dependent increase in ROS in isolated PVN neurons projecting to the spinal cord. Further, TNFα-mediated ROS production was heightened after AngII infusion. The finding that TNFR1 and gp91phox are positioned for rapid interactions, particularly in PVN-spinal cord projection neurons, provides a molecular substrate by which inflammatory signaling and oxidative stress may jointly contribute to AngII hypertension.

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来源期刊
Neurochemistry international
Neurochemistry international 医学-神经科学
CiteScore
8.40
自引率
2.40%
发文量
128
审稿时长
37 days
期刊介绍: Neurochemistry International is devoted to the rapid publication of outstanding original articles and timely reviews in neurochemistry. Manuscripts on a broad range of topics will be considered, including molecular and cellular neurochemistry, neuropharmacology and genetic aspects of CNS function, neuroimmunology, metabolism as well as the neurochemistry of neurological and psychiatric disorders of the CNS.
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