在慢性病中,BRCC36调节β-catenin的全方位化,以缓解血管化
Yalan Li1, Xiaoyue Chen1, Yiqing Xiong1
1Department of Nephrology, Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, #300 Guangzhou Road, 210029, China.
Journal of translational medicine
|September 3, 2024
概括
含BRCA1/BRCA2复杂子单元36 (BRCC36) 通过抑制Wnt/β-catenin通路,在慢性病 (CKD) 中保护血管化 (VC). 抑制BRCC36可能为CKD患者的VC提供一种新的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
背景情况:
- 血管化 (VC) 在慢性病 (CKD) 中普遍存在,而没有有效的药物治疗方法.
- 含BRCA1/BRCA2复杂子单元36 (BRCC36) 与骨质细胞分化有关,但其在VC中的作用尚不清楚.
研究的目的:
- 研究BRCC36在VC的发展中的作用和机制.
主要方法:
- 在人类和小鼠CKD模型和血管光滑肌细胞 (VSMCs) 中检查了BRCC36表达.
- 使用了功能增益和丧失实验,西式涂抹,qPCR,免疫光,免疫组织化学,共免疫沉和TOPFlash光酶试验.
- 研究了BRCC36.6对Wnt/β-catenin通路的调节.
主要成果:
- 从CKD患者和小鼠的化动脉和VSMC中减少了BRCC36的表达.
- 过度表达BRCC36缓解了VC,而耗尽则使其恶化,抑制了VSMC骨质分化.
- BRCC36通过减少β-catenin无化来抑制Wnt/β-catenin通路;皮奥格利塔增加了BRCC36并减弱了VC.
结论:
- BRCC36-β-catenin轴在VC病变发生过程中至关重要.
- 在CKD中,BRCC36和β-catenin是预防VC的潜在治疗点.
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