Phosphate-induced rat vascular smooth muscle cell calcification and the implication of zinc deficiency in a7r5 cell viability.
The calcification of vascular smooth muscle cells (VSMCs) is considered one of the major contributors for vascular disease. Phosphate is known as the inducer for VSMC calcification. In this study, we assessed whether phosphate affected cell viability and fetuin-A, a calcification inhibitor protein, both which are related to VSMC calcification. Also, VSMC viability by zinc level was assessed. The results showed that phosphate increased Ca and P deposition in VSMCs (A7r5 cell line, rat aorta origin). This phosphate-induced Ca and P deposition was consistent with the decreased A7r5 cell viability (P<0.05), which implies phosphate-induced calcification in A7r5 cells might be due to the decreased VSMC cell viability. As phosphate increased, the protein expression of fetuin-A protein was up-regulated. A7r5 cell viability decreased as the addition of cellular zinc level was decreased (P<0.05). The results suggested that zinc deficiency causes the decreased cell viability and it would be the future study to clarify how zinc does act for VSMC cell viability. The results suggest that the decreased VSMC viability by high P or low Zn in VSMCs may be the risk factor for vascular disease.
Department of Food Science and Nutrition, Andong National University, Gyeongbuk 760-749, Korea.
Mee-Young
MY
Shin
Department of Food Science and Nutrition, Andong National University, Gyeongbuk 760-749, Korea.
In-Sook
IS
Kwun
cell viability; fetuin-A; phosphate; rat vascular smooth muscle cell (VSMC); zinc