Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro.

BACKGROUND/AIMS: To investigate the effect of propranolol on cobalt chloride (CoCl2)-induced hypoxic proliferation in human umbilical vein endothelial cells (HUVECs).

METHODS: CoCl2 was administrated to HUVECs to mimic hypoxic proliferation in infantile hemangioma. The proliferation of HUVECs was detected by Cell Counting Kit-8. Effects of propranolol on apoptosis and expressions of cell cycle-related genes, CDK4 and cyclin D1, were detected by flow cytometry and RT-PCR respectively. The release of vascular endothelial growth factor (VEGF) and lactate dehydrogenase (LDH) was measured by enzyme-linked immunosorbent assay.

RESULTS: Propranolol significantly inhibited the CoCl2-induced hypoxic proliferation of HUVECs in a dose-dependent manner, and also induced apoptosis and suppressed the expression of CDK4 and cyclin D1. Propranolol also decreased the release of VEGF and LDH in the supernatant.

CONCLUSIONS: Propranolol could inhibit CoCl2-induced hypoxic proliferation of HUVECs through inducing apoptosis and cell cycle arrest.