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HAPLN1表现出双重效应:促进细胞外矩阵的恢复,同时增强关节炎性冠状细胞中的炎症媒介产量

Yunting Chen¹, Chenggen Luo¹, Kun Huang²

¹Department of Rheumatology and Immunology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.

|July 19, 2025

概括

氨酸和蛋白质甘氨酸链接蛋白1 (HAPLN1) 对炎症性肌肉细胞表现出双重作用,促进炎症,同时增强细胞活力和细胞外矩阵恢复. 这些效应与PI3K/AKT/mTOR通路激活有关.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
类风湿病学类风湿病学

背景情况:

纤维细胞样同胞细胞 (FLS) 所分泌的氨酸和蛋白质糖链接蛋白1 (HAPLN1),涉及炎症性关节炎的发病.
了解HAPLN1在冠状细胞中的作用对于开发针对性治疗炎症性关节疾病至关重要.

研究的目的:

调查HAPLN1对炎症冠状细胞的影响,并阐明其潜在的分子机制.
评估HAPLN1对细胞活力,增殖,炎症媒介产生的影响,以及细胞外矩阵成分的表达.

主要方法:

用IL-1β治疗的SW1353红细胞暴露于复合HAPLN1 (rHAPLN1).
特朗斯韦尔共同培养系统模拟了冠状细胞-FLS相互作用.
分析了细胞活力 (CCK-8),增殖 (EdU),基因表达 (RNA测序) 和蛋白质酸化 (西部斑).
生物信息分析确定了差异表达的基因和蛋白质-蛋白质相互作用.

主要成果:

HAPLN1增加了炎症介导体 (TNF-α,IL-6,MMPs,ADAMTS-5),但也增强了状细胞的活力和原II和TGF-β的表达.
生物信息学揭示了炎症通路的丰富以及ECM,TNF和IL-6通路的激活.
HAPLN1与ECM相互作用,与炎症相关的分子以及PI3K/AKT/mTOR通路的组件.
西方斑点证实在rHAPLN1治疗的红细胞中PI3K,AKT和mTOR的酸化升高.

结论:

HAPLN1在关节炎性冠状细胞中表现出双重作用,促进炎症,同时支持细胞活力和ECM恢复.
观察到的HAPLN1的影响与PI3K/AKT/mTOR信号通路的激活有关.
这些发现提供了关于HAPLN1对炎症性关节炎的复杂贡献的见解,并建议潜在的治疗点.

关键词:

细胞外矩阵 (ECM) 是一个细胞外矩阵.纤维细胞样同胞细胞 (FLS)氨酸和蛋白质甘油链接蛋白1 (HAPLN1)炎症的冠状细胞.炎症性关节炎是一种炎症性关节炎.在PI3K/AKT/mTOR路径中.

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