Gefitinib, as a new stent coating material, specifically inhibits smooth muscle cells proliferation through inhibition of EGFR/Akt pathway 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 μmol/L-10μmol/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.

The two facets of receptor tyrosine kinase in cardiovascular calcification—can tyrosine kinase inhibitors benefit cardiovascular system?

“…EGFR has an important role in VSMC proliferation and migration ( 32 ), as its inhibition mitigates proliferation and migration induced by balloon injury ( 33 ). A recent study has reported that TKI, gefitinib, can specifically inhibit VSMC proliferation by inhibiting EGFR-Akt phosphorylation ( 34 ).…”