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Cadmium induced endothelial dysfunction: Consequence of defective migratory pattern of endothelial cells in association with poor nitric oxide availability under cadmium challenge
Author(s) -
Kolluru Gopi Krishna,
Tamilarasan K.P.,
Priya S. Geetha,
Durgha N.P.,
Chatterjee Suvro
Publication year - 2006
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2006.02.002
Subject(s) - cadmium , angiogenesis , nitric oxide , cadmium chloride , microbiology and biotechnology , phalloidin , chemistry , cadmium oxide , endothelial stem cell , biology , biochemistry , cancer research , endocrinology , cytoskeleton , cell , in vitro , organic chemistry
Recent advances in cadmium toxicity research suggest an association between cadmium and vascular diseases. However, the mechanisms of cadmium implications in vascular diseases are not yet explained. The objective of our present study is to explore the mechanism of cadmium induced endothelial dysfunction. Doses of 0, 1 and 5 μM cadmium chloride were used to test the effects of cadmium on nitric oxide induced tube formation, cellular migration and subcellular actin polymerization in ECV‐304 endothelial cells. An egg‐yolk vascular bed model was used to study the effects of cadmium on angiogenesis. Results of the present study show that 5 μM cadmium chloride effectively inhibited angiogenesis, cellular migration and tube formation. Phalloidin staining, which represents actin polymerization of endothelial cells, reveals that cadmium induces an altered F‐actin pattern, which could be the prime cause for cadmium mediated inhibition of cellular migration and angiogenesis. Cadmium was also found to inhibit nitric oxide production in endothelial cells in a calcium free medium, which further hints that cadmium might impair endothelial functions by inhibiting endothelial nitric oxide synthase.