Inhibitory effect of iron on in vitro proliferation of smooth muscle cells.
- Author:
Chao WU
1
;
Hong QIU
;
Lian-jun XU
;
Jue YE
;
Zi-he YANG
;
Xin QIAN
;
Xian-min MENG
;
Yong-chun CUI
;
Li SONG
;
Run-lin GAO
Author Information
- Publication Type:Journal Article
- MeSH: Cell Proliferation; drug effects; Cells, Cultured; Dose-Response Relationship, Drug; Humans; Iron; pharmacology; Myocytes, Smooth Muscle; chemistry; drug effects; physiology; Proliferating Cell Nuclear Antigen; analysis; Tumor Suppressor Protein p53; analysis
- From: Chinese Medical Journal 2013;126(19):3728-3731
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDIron is a biocorrodible metal that might be used in bioabsorbable stents. This study investigated the effects at the cellular and protein levels of soluble divalent iron (ferrous gluconate) and soluble trivalent iron (ferric chloride) on the proliferation of human aortic smooth muscle cell (HASMC) in vitro.
METHODSThe water-soluble tetrazolium (WST-1) test was used to evaluate the effect of iron on proliferation of HASMC and Western blotting was used to measure the levels of signaling proteins involved in proliferative and apoptosis pathways.
RESULTSHASMC proliferation was inhibited in a concentration dependent manner after treatment with soluble divalent and trivalent iron at concentrations of 100-500 µmol/L. Western blotting analysis showed that the proliferating cell nuclear antigen (PCNA) expression following treatment with soluble divalent iron and trivalent iron at 100, 300 and 500 µmol/L was reduced compared to the control. The PCNA expression decreased with increasing iron concentration and to a greater extent with the trivalent iron than with the divalent iron treatment group. The p53 expression was markedly increased in a concentration dependent manner in both iron treatment groups.
CONCLUSIONThe soluble divalent iron and, to a greater degree trivalent iron, inhibited HASMC proliferation in a dosedependent manner, which may be attributed to reduction of PCNA expression and increase of p53 expression.