FAL1 regulates endothelial cell proliferation in diabetic arteriosclerosis through PTEN/AKT pathway

J. Shang, Q.-Z. Li, J.-Y. Zhang, H.-J. Yuan

Department of Endocrinology and Metabolism, Henan Provincial People’s Hospital, Zhengzhou University, Zhengzhou, Henan, PR China. lm1s3712@163.com

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• Metabolism

OBJECTIVE: This study aims to investigate the role of FAL1 in the occurrence and progression of diabetic arteriosclerosis and its underlying mechanism.

PATIENTS AND METHODS: FAL1 expression in coronary artery disease (CAD) tissues, normal artery tissues, and tumor necrosis factor-α (TNF-α)-induced endothelial cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The regulatory effects of FAL1 on cell proliferation, migration, and cell cycle were examined by cell counting kit-8 (CCK-8) assay, transwell assay, and flow cytometry, respectively. Western blot was used to detect protein expressions of proliferation-related gene PCNA (proliferating cell nuclear antigen), cell cycle-related genes cyclin D1, PTEN (phosphatase and tensin homolog deleted on chromosome ten) and AKT (protein kinase B) in HUVECs. Subsequently, rescue experiments were performed to assess whether PTEN/AKT signaling pathway is activated during the process of FAL1-regulated proliferation and migration of HUVECs.

RESULTS: FAL1 was highly expressed in CAD tissues and TNF-α-induced endothelial cells compared with that of controls. Overexpression of FAL1 in HUVECs promoted cell cycle, proliferation, and migration. FAL1 activated PTEN/AKT pathway in HUVECs, which was partially reversed by PTEN overexpression.

CONCLUSIONS: Highly expressed FAL1 can promote proliferation and migration of endothelial cells through activating PTEN/AKT signaling pathway.

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