Gefitinib, as a new stent coating material, specifically inhibits smooth muscle cells proliferation through inhibition of EGFR/Akt pathway phosphorylation
- DOI
- 10.2991/peee-15.2015.60How to use a DOI?
- Keywords
- Coating material, Cytotoxicity, Stent, Gefitinib, Smooth muscle cells, Phosphorylation.
- Abstract
The objective of this paper is to investigate the effects of gefitinib as a new stent coating material on proliferation of smooth muscle cells and the expression and phosphorylation of EGFR/Akt protein. Rat smooth muscle cells were cultured in medium with gefitinib (10-2 mol/L-10 mol/L) for 24h-72h. MTT assay was used to test the inhibition of cell proliferation. Western-blot was used to detect the expression of EGFR, Akt, phosphorylated EGFR (p-EGFR) and phosphorylated Akt (p-Akt). MTT assay showed that the inhibitory effect of gefitinib on smooth muscle cells’ proliferation was in a time and concentration dependent manner. Western-blot showed the expression of EGFR and Akt has no significant change between gefitinib group and paclitaxel group in smooth muscle cells, but gefitinib could significantly inhibit the phosphorylation of EGFR and Akt in smooth muscle cells compared with paclitaxel. It is concluded that Gefitinib could significantly suppress the proliferation of smooth muscle cells; the mechanism might be by inhibiting the phosphorylation of EGFR and Akt.
- Copyright
- © 2015, the Authors. Published by Atlantis Press.
- Open Access
- This is an open access article distributed under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/).
Cite this article
TY - CONF AU - F. Li AU - S.Y. Wang AU - J. Luo AU - Z.X. Wu AU - T. Xiao AU - O. Zeng AU - J. Yang AU - C. Chu PY - 2015/04 DA - 2015/04 TI - Gefitinib, as a new stent coating material, specifically inhibits smooth muscle cells proliferation through inhibition of EGFR/Akt pathway phosphorylation BT - Proceedings of the 2015 International Conference on Power Electronics and Energy Engineering PB - Atlantis Press SP - 225 EP - 227 SN - 2352-5401 UR - https://doi.org/10.2991/peee-15.2015.60 DO - 10.2991/peee-15.2015.60 ID - Li2015/04 ER -