Related Experiment Video
Updated: Apr 13, 2026

LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring
Published on: November 17, 2018
Atorvastatin counteracts high glucose-induced Krüppel-like factor 2 suppression in human umbilical vein endothelial
Yu-Sheng Liu1, Dong-Ling Xu, Zhi-Wei Huang
1Department of Cardiology, the Second Hospital of Shandong University , Shandong , PR China.
Objective:
Krüppel-like factor 2 (KLF2) is a transcription factor that regulates endothelial function and atorvastatin can stabilize atherosclerotic plaque and inhibit inflammation on endothelial cells by attenuating the role of cytokines. The aim of this study is to investigate the effect of high glucose (HG) on KLF2 expression in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms.
Methods:
HUVECs were isolated from the human umbilical cords from normal pregnancies and exposed to medium containing 25.5 mM D-glucose for 24 hours as the HG induction model (HG group). In the HG plus atorvastatin groups or KLF2 gene transduction, the medium then was collected for the nitric oxide (NO) assay and the cells were harvested for Western blot and for the real-time polymerase chain reaction to observe the expression of KLF2, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, total and phosphorylated endothelial NO synthase (eNOS), p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK)1/2, caspase-3 and cleaved caspase-3 and the role of the p38MAPK and ERK1/2 intracellular signal pathway. The cells' apoptosis was analyzed by flow cytometry.
Results:
HG dose-dependently increased apoptosis. The presence of HG inhibited the expression of KLF2 mRNA and protein in HUVECs and atorvastatin treatment increased KLF2 expression, thus counteracted HG-induced suppression of KLF2 expression, and overexpression of KLF2 might protect the cells from apoptosis. HG increased the expression of VCAM-1, ICAM-1, but decreased the nitric oxide release and the expression of p-eNOs/eNos in HUVECs. However, atorvastatin reversed these changes and also attenuated high-glucose induced p38 MAPK and ERK1/2 phosphorylation.
Conclusions:
HG suppressed the KLF2 expression in HUVECs. The suppression was counteracted by atorvastatin treatment, probably via attenuating the activation of the signal pathyway p38 MAPK and ERK1/2.
Related Concept Videos
Lipid-Lowering Drugs: Statins and Miscellaneous Agents
Glucose Absorption Into the Small Intestine
Hormones Regulating Blood Glucose
In addition to accelerating glucose uptake and utilization, insulin has...
Oral Hypoglycemic Agents: Biguanides and Glitazones
Glucose Homeostasis: Regulation of Blood Glucose
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors
Acarbose and miglitol are...

