人缺血病变中表达gpr17的少突胶质细胞前体的特征及其与反应性胶质反应的相关性。

IF 5.6 2区 医学 Q1 ONCOLOGY
The Journal of Pathology Pub Date : 2025-02-01 Epub Date: 2024-12-20 DOI:10.1002/path.6381
Stefano Raffaele, Bettina Hjelm Clausen, Francesca Carolina Mannella, Martin Wirenfeldt, Davide Marangon, Sarah Boe Tidgen, Silvia Corradini, Kirsten Madsen, Davide Lecca, Maria Pia Abbracchio, Kate Lykke Lambertsen, Marta Fumagalli
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引用次数: 0

摘要

缺血性脑卒中后,脑白质损伤和随后的脱髓鞘明显导致长期功能损害。发现新的药理学靶点,通过促进少突胶质前体细胞(OPCs)成熟为新的髓鞘少突胶质细胞来恢复髓鞘完整性,可能为缺血性卒中治疗开辟新的前景。在这方面,先前的研究强调了G蛋白偶联膜受体17 (GPR17)在脑损伤实验模型(包括缺血性卒中)中作为OPC分化的关键调节因子的作用。为了确定GPR17作为人类疾病背景下可能的靶标的翻译价值,我们利用免疫组织化学表征了缺血性卒中病例脑组织样本中表达GPR17的细胞的分布,并将其与邻近胶质细胞的反应状态相关联。结果表明,GPR17特异性修饰了由特殊标记物乳腺癌扩增序列1 (BCAS1)标记的具有分化倾向的OPCs亚群,该亚群在缺血事件发生后的后期积聚在梗死周围区域。有趣的是,表达gpr17的细胞的反应似乎与反应性小胶质细胞/巨噬细胞从吞噬型到营养不良表型的转换和星形细胞疤痕的形成是平行的。在女性受试者中,表达gpr17的OPCs与慢性缺血性病变周围的反应性小胶质/巨噬细胞和星形胶质细胞呈负相关,而在男性受试者中,这种关系不太明显。这些结果通过对公开的转录组数据集的生物信息学分析得到了加强,该数据集暗示了炎症和神经元与opc通信缺陷在缺血损伤后髓鞘再生失败中的可能作用。因此,这些数据加强了基于gpr17的髓鞘再生治疗与缺血性脑卒中治疗的相关性。©2024作者。《病理学杂志》由John Wiley & Sons Ltd代表大不列颠和爱尔兰病理学会出版。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Characterisation of GPR17-expressing oligodendrocyte precursors in human ischaemic lesions and correlation with reactive glial responses.

White matter damage and subsequent demyelination significantly contribute to long-term functional impairment after ischaemic stroke. Identifying novel pharmacological targets to restore myelin integrity by promoting the maturation of oligodendrocyte precursor cells (OPCs) into new myelinating oligodendrocytes may open new perspectives for ischaemic stroke treatment. In this respect, previous studies highlighted the role of the G protein-coupled membrane receptor 17 (GPR17) as a key regulator of OPC differentiation in experimental models of brain injury, including ischaemic stroke. To determine the translational value of GPR17 as a possible target in the context of human disease, we exploited immunohistochemistry to characterise the distribution of GPR17-expressing cells in brain tissue samples from ischaemic stroke cases and correlated it with the reactive state of neighbouring glial cells. The results showed that GPR17 specifically decorates a subpopulation of differentiation-committed OPCs, labelled by the peculiar marker breast carcinoma-amplified sequence 1 (BCAS1), that accumulates in the peri-infarct region in the later stages after the ischaemic event. Interestingly, the response of GPR17-expressing cells appears to be paralleled by the switch of reactive microglia/macrophages from a phagocytic to a dystrophic phenotype and by astrocytic scar formation. A negative correlation was found between GPR17-expressing OPCs and reactive microglia/macrophages and astrocytes surrounding chronic ischaemic lesions in female subjects, while the same relationship was less pronounced in males. These results were reinforced by bioinformatic analysis of a publicly available transcriptomic dataset, which implicated a possible role of inflammation and defective neuron-to-OPC communication in remyelination failure after ischaemic damage. Hence, these data strengthen the relevance of GPR17-based remyelinating therapies for the treatment of ischaemic stroke. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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来源期刊
The Journal of Pathology
The Journal of Pathology 医学-病理学
CiteScore
14.10
自引率
1.40%
发文量
144
审稿时长
3-8 weeks
期刊介绍: The Journal of Pathology aims to serve as a translational bridge between basic biomedical science and clinical medicine with particular emphasis on, but not restricted to, tissue based studies. The main interests of the Journal lie in publishing studies that further our understanding the pathophysiological and pathogenetic mechanisms of human disease. The Journal of Pathology welcomes investigative studies on human tissues, in vitro and in vivo experimental studies, and investigations based on animal models with a clear relevance to human disease, including transgenic systems. As well as original research papers, the Journal seeks to provide rapid publication in a variety of other formats, including editorials, review articles, commentaries and perspectives and other features, both contributed and solicited.
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