Comparing RNA-sequencing datasets from astrocytes, oligodendrocytes, and microglia in multiple sclerosis identifies novel dysregulated genes relevant to inflammation and myelination.

IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Sienna S Drake, Aliyah Zaman, Tristan Simas, Alyson E Fournier
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引用次数: 2

Abstract

Central nervous system (CNS) inflammation is a key factor in multiple sclerosis (MS). Invasion of peripheral immune cells into the CNS resulting from an unknown signal or combination of signals results in activation of resident immune cells and the hallmark feature of the disease: demyelinating lesions. These lesion sites are an amalgam of reactive peripheral and central immune cells, astrocytes, damaged and dying oligodendrocytes, and injured neurons and axons. Sustained inflammation affects cells directly located within the lesion site and further abnormalities are apparent diffusely throughout normal-appearing white matter and grey matter. It is only relatively recently, using animal models, new tissue sampling techniques, and next-generation sequencing, that molecular changes occurring in CNS resident cells have been broadly captured. Advances in cell isolation through Fluorescence Activated Cell Sorting (FACS) and laser-capture microdissection together with the emergence of single-cell sequencing have enabled researchers to investigate changes in gene expression in astrocytes, microglia, and oligodendrocytes derived from animal models of MS as well as from primary patient tissue. The contribution of some dysregulated pathways has been followed up in individual studies; however, corroborating results often go unreported between sequencing studies. To this end, we have consolidated results from numerous RNA-sequencing studies to identify and review novel patterns of differentially regulated genes and pathways occurring within CNS glial cells in MS. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology.

Abstract Image

Abstract Image

比较多发性硬化症中星形胶质细胞、少突胶质细胞和小胶质细胞的rna测序数据集,发现了与炎症和髓鞘形成相关的新的失调基因。
中枢神经系统(CNS)炎症是多发性硬化症(MS)的关键因素。由未知信号或信号组合引起的外周免疫细胞侵入中枢神经系统导致常驻免疫细胞的激活和疾病的标志性特征:脱髓鞘病变。这些病变部位是反应性外周和中枢免疫细胞、星形胶质细胞、受损和死亡的少突胶质细胞以及受损的神经元和轴突的混合体。持续的炎症影响直接位于病变部位的细胞,进一步的异常在正常的白质和灰质中弥漫性表现明显。直到最近,使用动物模型、新的组织取样技术和下一代测序技术,才广泛地捕捉到发生在中枢神经系统驻留细胞中的分子变化。通过荧光活化细胞分选(FACS)和激光捕获显微解剖分离细胞的进展,以及单细胞测序的出现,使研究人员能够研究来自多发性硬化症动物模型和原发患者组织的星形胶质细胞、小胶质细胞和少突胶质细胞基因表达的变化。一些失调通路的贡献在个体研究中得到了跟进;然而,在测序研究之间,证实的结果往往没有报道。为此,我们整合了大量rna测序研究的结果,以鉴定和回顾多发性硬化症中中枢神经胶质细胞内发生的差异调节基因和通路的新模式。
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来源期刊
WIREs Mechanisms of Disease
WIREs Mechanisms of Disease MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
11.40
自引率
0.00%
发文量
45
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