Different responses of cell cycle between rat vascular smooth muscle cells and vascular endothelial cells to paclitaxel.
10.1007/s11596-014-1285-1
- Author:
Liang JING
1
;
Xi PENG
;
Min-jie XIE
;
Zhi-yuan YU
;
Wei WANG
Author Information
1. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China, jingl7929@gmail.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Blotting, Western;
Cell Cycle;
drug effects;
Cell Cycle Proteins;
metabolism;
Cell Proliferation;
drug effects;
Cells, Cultured;
Cyclin B1;
metabolism;
Cyclin D1;
metabolism;
Cyclin-Dependent Kinase Inhibitor p21;
metabolism;
Cyclin-Dependent Kinase Inhibitor p27;
metabolism;
Endothelial Cells;
drug effects;
metabolism;
Flow Cytometry;
G1 Phase Cell Cycle Checkpoints;
drug effects;
Immunohistochemistry;
Microscopy, Fluorescence;
Muscle, Smooth, Vascular;
cytology;
Myocytes, Smooth Muscle;
drug effects;
metabolism;
Paclitaxel;
pharmacology;
Proliferating Cell Nuclear Antigen;
metabolism;
Rats;
Tubulin Modulators;
pharmacology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(3):370-375
- CountryChina
- Language:English
-
Abstract:
Although previous reports showed drug-eluting stent (DES) could effectively inhibit neointima formation, in-stent restenosis (ISR) remains an important obstacle. The purpose of this study was to investigate different effects of paclitaxel on proliferation and cell cycle regulators between vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs) of rats in vitro. The cultured VSMCs and VECs of rats from the same tissues were examined by using immunohistochemistry, flow cytometry and Western blotting in control and paclitaxel-treated groups. The results showed paclitaxel could effectively inhibit proliferation of VSMCs and VECs. However, as compared with VECs, proliferation of VSMCs in paclitaxel-treated group decreased less rapidly. The percentage of cells in G0-G1 and G2-M phases was reduced, and that in S phase increased after treatment for 72 h. The expression of cyclin D1 and B1, p27 and PCNA in VSMCs of paclitaxel-treated group was up-regulated, but that of p21 down-regulated as compared with VECs. It is concluded that there are significant differences in the expression of cell cycle regulators and proliferation rate between paclitaxel-treated VSMCs and paclitaxel-treated VECs, suggesting that the G1-S checkpoint regulated by paclitaxel may play a critical role in the development of complications of DES, which provides new strategies for treatments of ISR.
