Expression of CGRP in the Trigeminal Ganglion and Its Effect on the Polarization of Macrophages in Rats with Temporomandibular Arthritis.

IF 3.6 4区 医学 Q3 CELL BIOLOGY Cellular and Molecular Neurobiology Pub Date : 2024-02-16 DOI:10.1007/s10571-024-01456-7
Junli Tao, Xiaohui Wang, Jie Xu
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Abstract

Calcitonin gene-related peptide (CGRP) is synthesized and secreted by trigeminal ganglion neurons, and is a key neuropeptide involved in pain and immune regulation. This study investigates the expression of CGRP in the trigeminal ganglion (TG) and its regulatory role in the polarization of macrophages in rats with temporomandibular arthritis. A rat model of temporomandibular arthritis was established using CFA. Pain behavior was then observed. Temporomandibular joint (TMJ) and the TG were collected, and immunohistochemistry, immunofluorescence (IF) staining, and RT-qPCR were used to examine the expression of CGRP and macrophage-related factors. To investigate the impact of CGRP on macrophage polarization, both CGRP and its antagonist, CGRP 8-37, were separately administered directly within the TG. Statistical analysis revealed that within 24 h of inducing temporomandibular arthritis using CFA, there was a significant surge in CD86 positive macrophages within the ganglion. These macrophages peaked on the 7th day before beginning their decline. In this context, it's noteworthy that administering CGRP to the trigeminal ganglion can prompt these macrophages to adopt the M2 phenotype. Intriguingly, this study demonstrates that injecting the CGRP receptor antagonist (CGRP 8-37) to the ganglion counteracts this shift towards the M2 phenotype. Supporting these in vivo observations, we found that in vitro, CGRP indeed fosters the M2-type polarization of macrophages. CGRP can facilitate the conversion of macrophages into the M2 phenotype. The phenotypic alterations of macrophages within the TG could be instrumental in initiating and further driving the progression of TMJ disorders.

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三叉神经节中 CGRP 的表达及其对颞下颌关节炎大鼠巨噬细胞极化的影响
降钙素基因相关肽(CGRP)由三叉神经节神经元合成和分泌,是一种参与疼痛和免疫调节的关键神经肽。本研究探讨了 CGRP 在三叉神经节(TG)中的表达及其在颞下颌关节炎大鼠巨噬细胞极化中的调节作用。研究人员使用 CFA 建立了颞下颌关节炎大鼠模型。然后观察疼痛行为。收集颞下颌关节(TMJ)和TG,并采用免疫组织化学、免疫荧光(IF)染色和RT-qPCR检测CGRP和巨噬细胞相关因子的表达。为了研究 CGRP 对巨噬细胞极化的影响,分别在 TG 内直接注射 CGRP 及其拮抗剂 CGRP 8-37。统计分析表明,在使用CFA诱导颞下颌关节炎的24小时内,神经节内CD86阳性巨噬细胞显著激增。这些巨噬细胞在第7天达到峰值,然后开始下降。在这种情况下,值得注意的是,向三叉神经节注射 CGRP 可促使这些巨噬细胞采用 M2 表型。耐人寻味的是,这项研究表明,向神经节注射 CGRP 受体拮抗剂(CGRP 8-37)可抵消这种向 M2 表型的转变。为支持这些体内观察结果,我们发现在体外,CGRP 确实促进了巨噬细胞的 M2 型极化。CGRP 可促进巨噬细胞向 M2 表型转化。巨噬细胞在颞下颌关节内的表型改变可能有助于颞下颌关节疾病的发生和进一步发展。
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来源期刊
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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