Effects of atorvastatin on the mRNA and protein expression of ICAM‐1 and VCAM‐1 in cultured human umbilical vein endothelial cells
Zhiming Yang, Zhanhai Li, Chuanshi Xiao, Yun‐Fei Bian, Yu‐Ming Kang
Abstract
Zhiming Yang, Zhanhai Li, Chuanshi Xiao, Yun‐Fei Bian, Yu‐Ming Kang
Abstract
Intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) are important adhesion molecules. The present study was undertaken to observe effects of atorvastatin (ATV) on mRNA and protein expression of ICAM‐1 and VCAM‐1 in cultured human umbilical vein endothelial cells activated by tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β. The levels of mRNA (detected by RT‐PCR) and protein (measured by Western blot) of ICAM‐1 and VCAM‐1 increased initially after cells were coincubated with 10μg/L TNF‐α and IL‐1β (P<0.01), and reached peak with 30μg/L TNF‐α and IL‐1β; With 30μg/L TNF‐α and IL‐1β, mRNA and protein of ICAM‐1 and VCAM‐1 increased from 0h to 48h (P<0.01), and maintained high level until 72h. Compared with control, ICAM‐1 mRNA of TNF‐α, IL‐1β and ATV (10, 1.0, 0.1μmol/L) groups induced 2.23‐fold, 2.42‐fold,1.02‐fold (*P<0.05 vs TNF‐α or IL‐1β group), 1.36‐ fold* and 1.12‐fold* increases, respectively. Compared with control, VCAM‐1 mRNA of TNF‐α, IL‐1β and ATV (10, 1.0, 0.1 μmol/L) groups induced 2.35‐fold, 2.41‐fold, 1.10‐fold (*P<0.05 vs TNF‐α or IL‐1β group), 1.28‐fold* and 1.33‐fold* increases, respectively. The protein of ICAM‐1 and VCAM‐1 of TNF‐α and IL‐1β groups were higher than control (P<0.01), and ATV reduced (P<0.05) the increases in the protein of ICAM‐1 and VCAM‐1 induced by TNF‐α and IL‐1β. TNF‐α and IL‐1β dose‐dependently and time‐dependently induced increases in the mRNA and protein of ICAM‐1 and VCAM‐1, and ATV dose‐dependently reduced (P<0.05) the increases in the mRNA and protein of ICAM‐1 and VCAM‐1 induced by TNF‐α and IL‐1β. The results suggest that ATV increases the stability of plaques and slows down the progression of atherosclerosis.
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Intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) are important adhesion molecules. The present study was undertaken to observe effects of atorvastatin (ATV) on mRNA and protein expression of ICAM‐1 and VCAM‐1 in cultured human umbilical vein endothelial cells activated by tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β. The levels of mRNA (detected by RT‐PCR) and protein (measured by Western blot) of ICAM‐1 and VCAM‐1 increased initially after cells were coincubated with 10μg/L TNF‐α and IL‐1β (P<0.01), and reached peak with 30μg/L TNF‐α and IL‐1β; With 30μg/L TNF‐α and IL‐1β, mRNA and protein of ICAM‐1 and VCAM‐1 increased from 0h to 48h (P<0.01), and maintained high level until 72h. Compared with control, ICAM‐1 mRNA of TNF‐α, IL‐1β and ATV (10, 1.0, 0.1μmol/L) groups induced 2.23‐fold, 2.42‐fold,1.02‐fold (*P<0.05 vs TNF‐α or IL‐1β group), 1.36‐ fold* and 1.12‐fold* increases, respectively. Compared with control, VCAM‐1 mRNA of TNF‐α, IL‐1β and ATV (10, 1.0, 0.1 μmol/L) groups induced 2.35‐fold, 2.41‐fold, 1.10‐fold (*P<0.05 vs TNF‐α or IL‐1β group), 1.28‐fold* and 1.33‐fold* increases, respectively. The protein of ICAM‐1 and VCAM‐1 of TNF‐α and IL‐1β groups were higher than control (P<0.01), and ATV reduced (P<0.05) the increases in the protein of ICAM‐1 and VCAM‐1 induced by TNF‐α and IL‐1β. TNF‐α and IL‐1β dose‐dependently and time‐dependently induced increases in the mRNA and protein of ICAM‐1 and VCAM‐1, and ATV dose‐dependently reduced (P<0.05) the increases in the mRNA and protein of ICAM‐1 and VCAM‐1 induced by TNF‐α and IL‐1β. The results suggest that ATV increases the stability of plaques and slows down the progression of atherosclerosis.
Key concepts: Umbilical vein, VCAM-1, ICAM-1, Tumor necrosis factor alpha, Messenger RNA, Western blot, Molecular biology, Cell adhesion molecule