RNA-seq Based Transcriptome Analysis Reveals Role of Myoglobin in Rheumatoid Arthritis.

IF 4.5 2区 医学 Q2 CELL BIOLOGY Inflammation Pub Date : 2024-10-09 DOI:10.1007/s10753-024-02151-x
Haibin Wang, Xin Tian, Le Ji, Liang Shi, Ying Wang
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Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease which manifests as joint destruction and bone erosion, could be caused by both genetic and environmental factors. Currently, the causes of RA are unknown, and targeted therapies are often associated with side effects and contraindications. The detection rate of RA in women is higher than men (3:1), however, there is still a lack of comprehensive understanding of the relationship between sex and RA. We hypothesized gender differences in RA prevalence and their associated mechanisms by performing genome-wide transcriptome analysis of synovial biopsy samples. The results indicated that myoglobin (MB) was differentially expressed between males and females, with higher expression in males than females in healthy populations, while the opposite was observed in RA patients. MB interacted with HLA class II histocompatibility antigen, DM beta (HLA-DMB) and the inflammatory factor interleukin 6 (IL-6) in the human synovial cell line MH7A.

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基于 RNA-seq 的转录组分析揭示肌红蛋白在类风湿关节炎中的作用
类风湿性关节炎(RA)是一种慢性炎症性自身免疫性疾病,表现为关节破坏和骨侵蚀,可由遗传和环境因素引起。目前,类风湿性关节炎的病因尚不清楚,靶向治疗往往伴有副作用和禁忌症。女性 RA 的检出率高于男性(3:1),但人们对性别与 RA 的关系仍缺乏全面了解。我们通过对滑膜活检样本进行全基因组转录组分析,假设了RA发病率的性别差异及其相关机制。结果表明,肌红蛋白(MB)在男性和女性之间存在表达差异,在健康人群中男性的表达高于女性,而在RA患者中则相反。在人类滑膜细胞系 MH7A 中,MB 与 HLA II 类组织相容性抗原 DM beta(HLA-DMB)和炎症因子白细胞介素 6(IL-6)相互作用。
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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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