Octacosanol Enhances the Proliferation and Migration of Human Umbilical Vein Endothelial Cells via Activation of the PI3K/Akt and MAPK/Erk Pathways

• Published in: Lipids Vol. 50; no. 3; pp. 241 - 251
• Main Authors: Liu, Yu-Wei, Zuo, Pei-Yuan, Zha, Xiang-Nan, Chen, Xing-Lin, Zhang, Rong, He, Xiao-Xiao, Liu, Cheng-Yun
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.03.2015; Springer Nature B.V
• Subjects: Anticholesteremic Agents - pharmacology; Biomedical and Life Sciences; Cell Movement - drug effects; Cell Proliferation - drug effects; Cholesterol; Extracellular Signal-Regulated MAP Kinases - metabolism; Fatty Alcohols - pharmacology; Human umbilical vein endothelial cells; Human Umbilical Vein Endothelial Cells - cytology; Human Umbilical Vein Endothelial Cells - drug effects; Humans; Life Sciences; Lipidology; Lipids; MAPK/Erk1/2 signaling pathway; Medical Biochemistry; Medicinal Chemistry; Microbial Genetics and Genomics; Migration; Mitogen-Activated Protein Kinase Kinases - metabolism; Neurochemistry; Nutrition; Octacosanol; Oncogene Protein v-akt - metabolism; Original Article; Phosphatidylinositol 3-Kinases - metabolism; PI3K/Akt signaling pathway; Proliferation; p‐Akt; p‐Erk1/2; Signal Transduction; p-Erk1/2; Human umbilical vein endothelial cells; p-Akt; Octacosanol; Migration; MAPK/Erk1/2 signaling pathway; Proliferation; PI3K/Akt signaling pathway
• DOI: 10.1007/s11745-015-3991-2
• ISSN: 0024-4201

Atherosclerosis is characterized by endothelial dysfunction, lipid deposition, fibro-proliferative reactions and inflammation. Octacosanol is a high-molecular-weight primary aliphatic alcohol. As the main component of a cholesterol-lowering drug, octacosanol could inhibit lipids accumulation and cholesterol metabolism. To explore the indication of octacosanol on endothelial protection, we evaluated its effects on the proliferation and migration of human umbilical vein endothelial cells (HUVEC). Cell viability assay using methyl thiazolyl tetrazolium and 5-ethynyl-2′-deoxyuridine revealed that 3.125 μg/ml octacosanol promoted the proliferation of HUVEC. A cell migration assay indicated that 0.781 and 3.125 μg/ml octacosanol increased the migration of HUVEC. Moreover, the phosphorylation levels of Akt and Erk1/2 were significantly elevated under exposure to octacosanol. Blocking the activation of Akt and Erk with their potent inhibitors LY294002 and PD98059, respectively, markedly attenuated the octacosanol-induced proliferation and migration of HUVEC. These findings demonstrated for the first time that octacosanol enhanced the proliferation and migration of HUVEC and mediated these effects through activation of the PI3K/Akt and MAPK/Erk1/2 signaling pathways.