在糖尿病肺部损伤中因高血糖引起的单细胞粘合剂氨酸矩阵
Andrew Jun Wang1, Juan Ren1, Aimin Wang1
1Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, USA.
The Journal of biological chemistry
|July 2, 2023
概括
呼吸道平滑肌肉细胞中的高葡萄糖增加了 hialuronan,促进炎症细胞粘附和糖尿病肺部损伤. 这种机制涉及瘤亡因子刺激的基因-6和重链修饰的氨酸.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 糖尿病学 糖尿病学
背景情况:
- 糖尿病肺部损伤涉及炎症单细胞和巨细胞.
- 这些细胞在糖尿病肺部损伤中的透机制尚不清楚.
研究的目的:
- 阐明气道光滑肌细胞 (SMCs) 在高血糖条件下调解单细胞粘附的机制.
- 调查氨酸 (HA) 和瘤亡因子刺激基因-6 (TSG-6) 在这个过程中的作用.
主要方法:
- 在高葡萄糖条件下 (25.6 mM) 培养了气道光滑肌肉细胞.
- 进行了单细胞 (U937) 粘附测试.
- 分析了氨的合成和修饰 (重链-HC).
- 在体外研究了TSG-6表达及其与HA的相互作用.
主要成果:
- 高葡萄糖显著增加了SMCs的氨酸产量,增强了单细胞粘附.
- 在高葡萄糖条件下,瘤亡因子刺激的基因-6表达增加.
- 在单细胞粘合电缆上观察到重链修饰的氨酸结构.
- 氨酸治疗放大了HA合成和HC修饰的HA结构.
结论:
- 呼吸道光滑肌中的高血糖会诱导氨酸的合成,为炎症细胞创造一个粘合基质.
- 这一过程导致慢性炎症,纤维化和糖尿病肺部损伤.
- TSG-6和HC修饰的HA在单细胞招募中发挥作用.
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