巨细胞β2-AR激活通过通过cAMP/PKA/CREB通路调高Trem1来放大伤口愈合中的炎症
Huawei Wei1, Mengqiu Deng1, Ruifeng Ding1
1Department of Anesthesiology, Changzheng Hospital, Second Affiliated Hospital of Naval Medical University, Shanghai 200003, China.
International immunopharmacology
|January 8, 2024
概括
β-2 上腺素受体 (β2-AR) 激活通过通过cAMP/PKA/CREB通路调节肌肉细胞1 (Trem1) 上表达的触发受体,从而放大炎症并阻碍伤口愈合.
科学领域:
- 免疫学 免疫学 免疫学
- 伤口愈合 治愈 伤口愈合
- 分子生物学分子生物学
背景情况:
- 炎症是伤口愈合的重要组成部分.
- 上腺素通过β2-上腺素受体 (β2-AR) 调节炎症.
- 在伤口愈合炎症中β2-AR的精确分子机制尚不清楚.
研究的目的:
- 研究β2-AR在伤口愈合炎症中的作用.
- 阐明在伤口愈合期间参与β2-AR介导炎症的分子途径.
主要方法:
- 伤口和巨细胞转录组数据集的生物信息再分析.
- 小鼠后腿脚下部伤口模型用于体内评估.
- 在实验室测试使用RAW细胞,siRNA淘汰Trem1,西部斑,qPCR和cAMP通路调节器.
主要成果:
- 在骨髓细胞1 (Trem1) 上表达的触发受体在受伤后通过巨细胞β2-AR激活升高调节.
- β2-AR激动剂损害了伤口愈合,增加了Trem1,促炎细胞因子,并激活了cAMP/PKA/CREB通路.
- 巨细胞β2-AR激活放大了LPS诱导的炎症;Trem1倒置逆转了这一效应,通过cAMP/PKA/CREB通路证实了它的作用.
结论:
- β2-AR激动剂通过上调Trem1.1,加剧炎症并阻碍伤口愈合.
- 在巨细胞中β2-AR激活会通过cAMP/PKA/CREB通路诱导Trem1的表达.
- 准β2-AR或Trem1可能为伤口愈合提供治疗策略.
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