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表达 PLP1 的周围神经 DRG 细胞促进涉及 DRG 神经元中 Piezo2 上调的结肠和躯体慢性机械性疼痛。

Plp1-expresssing perineuronal DRG cells facilitate colonic and somatic chronic mechanical pain involving Piezo2 upregulation in DRG neurons.

机构信息

Department of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298-0551, USA.

Department of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298-0551, USA.

出版信息

Cell Rep. 2024 May 28;43(5):114230. doi: 10.1016/j.celrep.2024.114230. Epub 2024 May 13.

DOI:10.1016/j.celrep.2024.114230
PMID:38743566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11234328/
Abstract

Satellite glial cells (SGCs) of dorsal root ganglia (DRGs) are activated in a variety of chronic pain conditions; however, their mediation roles in pain remain elusive. Here, we take advantage of proteolipid protein (PLP)/creER-driven recombination in the periphery mainly occurring in SGCs of DRGs to assess the role of SGCs in the regulation of chronic mechanical hypersensitivity and pain-like responses in two organs, the distal colon and hindpaw, to test generality. We show that PLP/creER-driven hM3Dq activation increases, and PLP/creER-driven TrkB.T1 deletion attenuates, colon and hindpaw chronic mechanical hypersensitivity, positively associating with calcitonin gene-related peptide (CGRP) expression in DRGs and phospho-cAMP response element-binding protein (CREB) expression in the dorsal horn of the spinal cord. Activation of Plp1 DRG cells also increases the number of small DRG neurons expressing Piezo2 and acquiring mechanosensitivity and leads to peripheral organ neurogenic inflammation. These findings unravel a role and mechanism of Plp1 cells, mainly SGCs, in the facilitation of chronic mechanical pain and suggest therapeutic targets for pain mitigation.

摘要

背根神经节（DRG）中的卫星胶质细胞（SGCs）在多种慢性疼痛情况下被激活；然而，它们在疼痛中的介导作用仍不清楚。在这里，我们利用蛋白脂质蛋白（PLP）/creER 在周围的驱动重组，主要发生在 DRG 的 SGCs 中，以评估 SGC 在调节慢性机械性超敏反应和两个器官（远端结肠和后爪）疼痛样反应中的作用，以测试普遍性。我们表明，PLP/creER 驱动的 hM3Dq 激活增加，而 PLP/creER 驱动的 TrkB.T1 缺失减弱了结肠和后爪的慢性机械性超敏反应，与 DRG 中的降钙素基因相关肽（CGRP）表达和脊髓背角中的磷酸环磷腺苷反应元件结合蛋白（CREB）表达呈正相关。Plp1 DRG 细胞的激活还增加了表达 Piezo2 并获得机械敏感性的小 DRG 神经元的数量，并导致外周器官神经原性炎症。这些发现揭示了 Plp1 细胞（主要是 SGCs）在促进慢性机械性疼痛中的作用和机制，并为缓解疼痛提供了治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/780bc4dfbb8c/nihms-2000467-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/1358bb5b49fe/nihms-2000467-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/2a952149b501/nihms-2000467-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/021431e52c00/nihms-2000467-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/b2318f8ae5db/nihms-2000467-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/9c6318d407d0/nihms-2000467-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/8c303ffac392/nihms-2000467-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/780bc4dfbb8c/nihms-2000467-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/1358bb5b49fe/nihms-2000467-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/2a952149b501/nihms-2000467-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/021431e52c00/nihms-2000467-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/b2318f8ae5db/nihms-2000467-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/9c6318d407d0/nihms-2000467-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/8c303ffac392/nihms-2000467-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/209a/11234328/780bc4dfbb8c/nihms-2000467-f0008.jpg

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