TRAF6 mediates high glucose-induced endothelial dysfunction

Experimental Cell Research
Rong LiuFang Liu

Abstract

To investigate the role of tumor necrosis factor-associated factor 6 (TRAF6) in high glucose-induced endothelial cell dysfunction. Human aortic endothelial cells (HAECs) were cultured in high glucose medium, and TRAF6 expression was assayed by quantitative real-time Polymerase Chain Reaction (PCR) and western blotting. The effect of TRAF6 on in vitro endothelial cell viability, apoptosis, migration, and endothelial-monocyte adhesion was investigated by gene knockdown. The expression of TRAF6 and related adhesion molecules was assayed in a mouse streptozotocin-induced type I diabetes model. The signaling pathways associated with TRAF6 effects on endothelial cells were investigated in high glucose HAEC cultures. Culture of HAECs in high glucose medium significantly increased TRAF6 mRNA and protein expression in a time dependent manner. High glucose markedly reduced HAEC viability, apoptosis, and migration, and these effects was significantly reversed by TRAF6 knockdown. High glucose significantly increased intercellular adhesion of THP-1 monocytic cells and HAECs via upregulation of ICAM-1 and VCAM-1 expression, and TRAF6 knockdown attenuated the effect on THP-1 cell adhesion. TRAF6, ICAM-1, and VCAM-1 expression were increased i...Continue Reading

Citations

Dec 24, 2018·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Yan-Hui ShenFei-Hua Wu
Dec 1, 2020·Journal of Alzheimer's Disease : JAD·Haripriya Vittal RaoPaula Grammas
Apr 4, 2021·Molecular and Cellular Biochemistry·Ampadu O JacksonShiyin Long
May 8, 2021·Endocrinología, Diabetes Y Nutrición·Aziguli KasimuXiangling Zhou

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