TUG1 promotes diabetic atherosclerosis by regulating proliferation of endothelial cells via Wnt pathway

H.-Y. Yan, S.-Z. Bu, W.-B. Zhou, Y.-F. Mai

Department of Endocrinology, The Affiliated Hospital of Medical School, Ningbo Universtiy, Ningbo, China. nbmyf@msn.com

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• Metabolism

OBJECTIVE: To explore the specific role of TUG1 in regulating the occurrence and progression of diabetic atherosclerosis and its underlying mechanism.

PATIENTS AND METHODS: TUG1 expressions in coronary artery disease (CAD) tissues, normal arterial tissues, endothelial cells induced by high-dose glucose and tumor necrosis factor-α (TNF-α) were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The effects of TUG1 on proliferation, migration and cell cycle of human umbilical vein endothelial cells (HUVECs) were detected by cell counting kit-8 (CCK-8), transwell assay and flow cytometry, respectively. Subsequently, protein expressions of proliferation-related genes, cell cycle-related genes and Wnt pathway-related genes were detected by Western blot after altering TUG1 expression in HUVECs. Further rescue experiments were carried out to explore whether TUG1 could regulate diabetic atherosclerosis via Wnt pathway.

RESULTS: Overexpressed TUG1 was found in CAD tissues and endothelial cells induced by high-dose glucose and TNF-α compared with those of controls. TUG1 overexpression remarkably promoted proliferation, migration and cell cycle of HUVECs. Protein expressions of β-catenin and c-Myc were upregulated by overexpression of TUG1. Rescue experiments indicated that XAV-939, the inhibitor of Wnt pathway, could partially reverse the increased proliferative and migratory changes in HUVECs induced by TUG1 overexpression.

CONCLUSIONS: We found that overexpressed TUG1 stimulates proliferation and migration of endothelial cells via Wnt pathway, thereby promoting the occurrence and progression of diabetic atherosclerosis.

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