SET8 suppression mediates high glucose-induced vascular endothelial inflammation via the upregulation of PTEN

• Main Authors: Xuefang Shen, Xiangyuan Chen, Jing Wang, Jing Liu, Zhiyao Wang, Qing Hua, Qichao Wu, Yanguang Su, Huanzhong He, Yuqin Hu, Zhipeng Meng, Wanxia Xiong, Minmin Zhu
• Format: Article
• Language: English
• Published: Nature Publishing Group 2020-10-01
• Series: Experimental and Molecular Medicine
• Online Access: https://doi.org/10.1038/s12276-020-00509-3
• ISSN: 1226-3613; 2092-6413

Diabetes: Protein modulators of vascular inflammation High glucose levels in patients with diabetes trigger vascular inflammation by affecting the expression of key proteins in blood vessel linings. Elevated glucose causes inflammation of the endothelium, a thin layer of cells that lines blood and lymph vessels, leading to cardiovascular complications. The phosphatase and tensin homolog protein (PTEN) contributes to endothelial inflammation, but the precise mechanisms are unclear. Xuefang Shen at Fudan University in Shanghai, China, and co-workers demonstrated that elevated glucose increases PTEN expression, with increased levels of the protein found in peripheral blood cells of diabetic patients and aortic tissues of diabetic rats. In further experiments on rats, the researchers found that glucose also suppressed another protein called SET8, which contributed to increased PTEN levels. This suggests that SET8 is involved in PTEN modulation, and that both proteins influence vascular inflammation.