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小胶质细胞 TNFα 在神经病理性疼痛期间诱导脊髓内皮细胞中 COX2 和 PGI2 合酶的表达。

Microglial TNFα Induces COX2 and PGI2 Synthase Expression in Spinal Endothelial Cells during Neuropathic Pain.

机构信息

Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.

出版信息

eNeuro. 2017 Apr 21;4(2). doi: 10.1523/ENEURO.0064-17.2017. eCollection 2017 Mar-Apr.

DOI:10.1523/ENEURO.0064-17.2017
PMID:28451639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5399753/
Abstract

Prostaglandins (PGs) are typical lipid mediators that play a role in homeostasis and disease. They are synthesized from arachidonic acid by cyclooxygenase 1 (COX1) and COX2. Although COX2 has been reported to be upregulated in the spinal cord after nerve injury, its expression and functional roles in neuropathic pain remain unclear. In this study, we investigated the expression of Cox2, PGI2 synthase (Pgis), and prostaglandin I2 receptor (IP receptor) mRNA in the rat spinal cord after spared nerve injury (SNI). Levels of Cox2 and Pgis mRNA increased in endothelial cells from 24 to 48 h after nerve injury. IP receptor mRNA was constitutively expressed in dorsal horn neurons. A COX2 inhibitor and IP receptor antagonists attenuated pain behavior in the early phase of neuropathic pain. Furthermore, we examined the relationship between COX2 and tumor necrosis factor-α (TNFα) in the spinal cord of a rat SNI model. Levels of TNFα mRNA transiently increased in the spinal microglia 24 h after SNI. The TNF receptors Tnfr1 and Tnfr2 mRNA were colocalized with COX2. Intrathecal injection of TNFα induced Cox2 and Pgis mRNA expression in endothelial cells. These results revealed that microglia-derived TNFα induced COX2 and PGIS expression in spinal endothelial cells and that endothelial PGI2 played a critical role in neuropathic pain via neuronal IP receptor. These findings further suggest that the glia-endothelial cell interaction of the neurovascular unit via transient TNFα is involved in the generation of neuropathic pain.

摘要

前列腺素（PGs）是典型的脂质介质，在维持内环境稳定和疾病中发挥作用。它们由环氧合酶 1（COX1）和 COX2 从花生四烯酸合成。虽然有报道称 COX2 在神经损伤后脊髓中上调，但它在神经病理性疼痛中的表达和功能作用仍不清楚。在这项研究中，我们研究了 spared nerve injury（SNI）后大鼠脊髓中 Cox2、PGI2 合酶（Pgis）和前列腺素 I2 受体（IP 受体）mRNA 的表达。神经损伤后 24 至 48 小时，内皮细胞中 Cox2 和 Pgis mRNA 水平增加。IP 受体 mRNA 在背角神经元中持续表达。COX2 抑制剂和 IP 受体拮抗剂可减轻神经病理性疼痛早期的疼痛行为。此外，我们在大鼠 SNI 模型的脊髓中检查了 COX2 和肿瘤坏死因子-α（TNFα）之间的关系。SNI 后 24 小时，脊髓小胶质细胞中 TNFα mRNA 水平短暂增加。TNF 受体 Tnfr1 和 Tnfr2 mRNA 与 COX2 共定位。鞘内注射 TNFα可诱导内皮细胞中 Cox2 和 Pgis mRNA 的表达。这些结果表明，小胶质细胞衍生的 TNFα诱导脊髓内皮细胞中 COX2 和 PGIS 的表达，内皮 PGI2 通过神经元 IP 受体在神经病理性疼痛中发挥关键作用。这些发现进一步表明，通过瞬态 TNFα的神经血管单元的神经胶质细胞-内皮细胞相互作用参与了神经病理性疼痛的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fb9/5399753/6f6f8f5107c1/enu0021722900009.jpg
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