• Shuming Chen, Xuekai Zhao, Junjie Huang, Na Lin, Qianhui Xu, Jianwei Chen, Jianqiang Huang, Lie Wang, Chen Lin, and Zaizhong Zhang.
• Department of General Surgery, 900th Hospital of the Joint Logistics Support Force (Dongfang Hospital of Xiamen University, School of Medicine, Xiamen University; Fuzhou General Hospital of Fujian Medical University), Fuzhou, Fujian, China.
• Medicine (Baltimore). 2023 Aug 11; 102 (32): e34672e34672.

BackgroundPropranolol is the first choice for treating infantile hemangioma (IH). How propranolol works in IH remains unclear. Infantile hemangioma endothelial cells (HemECs) express Notch1, Jagged, Hey1, and other molecules in the Notch pathway, suggesting that Notch pathway-related molecules play an important role in affecting vascular endothelial cell proliferation. Whether propranolol can affect the Notch signaling pathway in IH treatment is unclear.MethodsWe performed this study to observe the effect of propranolol on the expression of Notch signaling pathway molecules in human umbilical vein endothelial cells (HUVECs) and to explore the therapeutic mechanism of propranolol on IH. HUVECs cultured in vitro were exposed to 60, 120, 240, 360, or 480 µM propranolol. The morphological changes of the HUVECs were observed under an inverted microscope. HUVECs proliferation was detected with Cell Counting Kit-8 (CCK-8). The effects of propranolol on HUVECs apoptosis were detected by flow cytometry. The role of Notch in propranolol inhibition of HUVEC proliferation was analyzed with real-time polymerase chain reaction (PCR) and western blotting.ResultsPropranolol reduced HUVECs numbers and altered their morphology. The inhibitory effect of propranolol on cell proliferation was dependent on the reaction time and drug concentration. Propranolol upregulated Jagged1, Notch1, and Hey1 expression and downregulated delta-like ligand4 (DLL4) expression.ConclusionsPropranolol may play a role in IH treatment by increasing Jagged1 expression in endothelial cells, activating the Notch pathway and inducing the upregulation of the downstream target gene HEY1.Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.

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