Protective effect of endoplasmic reticulum stress on calcification of VSMCs induced by high glucose and its effect on expression of GRP78, CHOP, and Caspase-12

This article investigates the role of endoplasmic reticulum stress (ERS) in high-glucose-induced vascular smooth muscle cells (VSMCs) calcification and to explore its effects on the expression of GRP78, CHOP, and Caspase-12.VSMCs were treated with high glucose (35 mmoL/L) to induce diabetes to see whether high glucose can induce ERS. Changes in alkaline phosphatase activity, calcium deposition, and runt-related transcription factor 2 (Runx2) were measured. After 5 days’ treatment, the alkaline phosphatase activity, calcium content, and Runx2 expression of the bone differentiation marker protein were all up-regulated in the β-glycerophosphate group, the high-glucose group, and the β-glycerophosphate + high-glucose group when compared with the control group. High-glucose treatment of VSMCs can cause ERS and apoptosis and induces transdifferentiation of VSMCs into osteoblast-like cells, resulting in increased basal phosphatase activity, up-regulation of calcium content, and bone differentiation markers in VSMCs. The findings confirm that ERS plays an important role in the calcification of VSMCs.