Interactions between cultured bovine arterial endothelial and smooth muscle cells; effects of modulated low density lipoproteins on cell proliferation and prostacyclin release.

We exposed bovine aortic endothelial cells in culture to native LDL (n-LDL) and LDL modulated by dimethylsulfoxide (DMSO-LDL), dimethylsulfoxide-soluble particles from cigarette smoke (DSP-LDL) or Cu2+ (Cu(2+)-LDL) to explore the hypothesis that these LDL-forms might influence interactions between endothelial and smooth muscle cells. It was shown that 3H-thymidine incorporation into endothelial cells was decreased by DMSO-LDL, DSP-LDL and Cu(2+)-LDL compared to n-LDL, while it was higher by DSP-LDL compared to its control i.e. DMSO-LDL. These effects could be transferred by conditioned medium to smooth muscle cell cultures. DSP-LDL or Cu(2+)-LDL decreased total cellular protein of endothelial cells. Initial (15 min) prostacyclin release from endothelial cells was increased by all LDL preparations compared to medium without LDL, most pronounced for Cu(2+)-LDL. If n-LDL was control, only Cu(2+)-LDL significantly increased the release of prostacyclin during 15 min and during 24 h. The release of prostacyclin assayed after 24 h was depressed by DSP-LDL compared to DMSO-LDL. This study demonstrated that interactions between endothelial and smooth muscle cells could be influenced by LDL treated by dimethylsulfoxide-soluble particles from cigarette smoke or by Cu2+, and their effects were not similar. DSP-LDL, in contrast to Cu(2+)-LDL, significantly decreased the release of prostacyclin by endothelial cells after 24 h incubations and via endothelial cell conditioned medium stimulated smooth muscle cell proliferation judged by increased 3H-thymidine incorporation. The results might be of relevance for atherogenesis.