Effects of S100A12 reduction on H2O2-induced injury of human vascular smooth muscle cells (HVSMCs).

ABSTRACT

Thoracic aortic dissection is a catastrophic acute aortic disease with a high postoperative mortality. Although TAD results from various risk factors, the final common pathway for its development is tunica media dysfunction with vascular inflammation. The aim of the present study was to investigate the protective effects of S100A12 reduction on hydrogen peroxide (H2O2)-induced human vascular smooth muscle cells (HVSMCs) injury and evaluate the relevance of S100A12 and aortic disease. In this study, HVSMCs were exposed to the H2O2 in the presence or absence of S100A12, then cell viability was detected by MTT assay, cell apoptosis was performed with the flow cytometry kit, IL-6 and TNFα production evaluated by ELISA and apoptotic proteins were investigated by western blot. The results showed that H2O2 inhibited cell proliferation, induced cell apoptosis, IL-6 and TNFα release, the increase of caspase-3 protein and the decrease of Bcl-2, while transfection with S10012A shRNA significantly repaired the situation above. Our findings suggested that reduction of S100A12 protects HVSMCs against H2O2-induced injury, and may be useful as a treatment for aortic disease.