上腺素通过PKC/NFκB介导的NOX2上调节促进了血管前进性纤维细胞中的氧化应激
Yi-Ming Wang1, Hong-Ke Dong1, Min Dai1
1Department of Physiology, Nanjing Medical University, Nanjing, People's Republic of China.
Redox report : communications in free radical research
|April 24, 2025
概括
上腺素 (NE) 通过氧化应激驱动血管顺序性纤维细胞 (VAF) 的增殖和迁移. 这一过程涉及NADPH氧化酶2 (NOX2) 激活,由α受体,蛋白激酶C (PKC) 和NF-kappaB (NFκB) 介导.
科学领域:
- 心血管生物学 心血管生物学
- 血管生理学 血管生理学
- 细胞信号传输 细胞信号传输
背景情况:
- 交感过度活跃与血管重塑有关,交感纤维主要透动脉道.
- 血管附带纤维细胞 (VAFs) 是血管重塑过程中的关键参与者.
- 连接同情过度活动与VAF扩散和迁移的具体机制尚不清楚.
研究的目的:
- 为了研究同情性过度活性的影响,模拟的诺拉上腺素 (NE),在VAF的增殖和迁移.
- 阐明 NE 诱导的 VAF 反应中涉及的信号通路.
主要方法:
- 血管顺序性纤维细胞 (VAFs) 从大鼠胸前动脉中分离出来.
- 模拟的交感性过度活跃通过应用北上腺素 (NE) 到VAFs.
- 评估了NE和各种抑制剂 (NOX抑制剂,上腺受体对抗剂,PKC和NFκB抑制剂) 对VAF的影响.
主要成果:
- 上腺素 (NE) 增加了NADPH氧化酶2 (NOX2) 表达和超氧化物产生,主要由α-上腺受体介导.
- NE诱导的VAF增殖和迁移被NOX2抑制和超氧化物清理减弱.
- NE促进了蛋白激酶C (PKC) 酸化和NFκB核转移,这对于NOX2激活和VAF扩散/迁移至关重要.
结论:
- 上腺素 (NE) 通过α受体/PKC/NFκB通路刺激氧化应激,导致NOX2上调.
- 这种NE诱导的氧化应激显著促进了血管顺序性纤维细胞 (VAF) 的增殖和迁移.
- 针对这种途径可能为涉及交感过度活动和血管重塑的疾病提供治疗策略.
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