通过调节JAK2/STAT3信号传递,CLCF1有助于高葡萄糖诱导的EndMT
Rongrong Deng1,2, Kaiying He3, Qicai You1,2
1Lanzhou University, Lanzhou, 730030, Gansu, China.
心脏类型细胞因子1 (CLCF1) 通过JAK2/STAT3通路促进内皮细胞转移到介质酶体 (EndMT) 来驱动糖尿病病的进展. 准CLCF1可能为DKD提供一种新的治疗策略.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 分子生物学分子生物学
- 内分泌学 在内分泌学.
背景情况:
- 心脏类型细胞因子1 (CLCF1) 涉及到质白蛋白透性和蛋白尿症.
- 目前尚不清楚CLCF1在糖尿病病 (DKD) 发病过程中的具体作用.
研究的目的:
- 在DKD的背景下,研究CLCF1在内皮转移到介质细胞转换 (EndMT) 中的机制作用.
- 为了阐明JAK2/STAT3信号通路在CLCF1-介导的EndMT中的参与.
主要方法:
- 在DKD患者和高葡萄糖 (HG) 刺激的人类球内皮细胞 (HRGECs) 中使用qRT-PCR,西斑和IHC.量化CLCF1表达.
- 评估了CLCF1对HG诱导的EndMT和JAK2/STAT3信号的影响.
- 使用JAK2/STAT3激动剂 (科利维林) 来检查CLCF1-敲击HRGEC中的通路激活.
主要成果:
- 在DKD患者和HG治疗的HRGEC患者中,CLCF1表达显著升高.
- CLCF1敲击减弱了HG诱导的EndMT,降低了α-平滑肌肉动因素 (α-SMA) 和维敏水平.
- 过度表达CLCF1促进了EndMT并激活了JAK2/STAT3通路;可利维林逆转了CLCF1敲击的保护作用.
结论:
- 在HRGEC中,CLCF1通过调节JAK2/STAT3通路来调节高葡萄糖诱导的EndMT.
- CLCF1/JAK2/STAT3信号轴是糖尿病病的发病过程中的关键参与者.
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