HDAC11通过诱导THP-1细胞和PBMC中的YAP表达来调节Palmitate诱导的NLRP3炎症酶激活
Hye-Eun Byeon1, Sung-E Choi2, Yujin Kim3,4
1Institute of Medical Science, Ajou University School of Medicine, Suwon, Gyeonggi-do 16499, Republic of Korea.
Endocrinology
|February 17, 2024
概括
海斯脱乙酶11 (HDAC11) 通过激活NLRP3炎症体来驱动肥胖症的炎症. 抑制HDAC11减少了这种激活,为代谢疾病提供了潜在的治疗策略.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 代谢疾病 代谢疾病
背景情况:
- 海斯脱乙酶11 (HDAC11) 与代谢疾病和慢性炎症有关.
- HDAC11在棕酸 (PA) 诱导的炎症和NLRP3炎症酶激活中的作用尚不清楚.
研究的目的:
- 研究PA对HDAC11活性和NLRP3炎症酶激活的影响.
- 探索HDAC11在PA诱导的NLRP3炎症酶激活中的作用及其与YAP的关系.
主要方法:
- 人类外周血液单核细胞和THP-1细胞被用PA治疗.
- 评估了HDAC11活性和NLRP3炎症酶标志物.
- 使用FT895抑制了HDAC11或使用siRNA减少.
- 研究了HDAC11,YAP和NLRP3之间的相互作用.
主要成果:
- PA治疗增加了HDAC11活性和NLRP3炎症酶激活,包括NLRP3表达,caspase-1 p10激活和IL-1β产生.
- 抑制HDAC11 (FT895或siHDAC11) 减弱了PA诱导的NLRP3炎症酶激活.
- PA诱导了YAP表达及其与NLRP3的相互作用,NLRP3通过HDAC11抑制被阻止.
结论:
- 在PA诱导的NLRP3炎症酶激活中,HDAC11起着至关重要的作用.
- 抑制HDAC11是一种潜在的治疗方法,用于与肥胖相关的炎症.
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