NALP3is Activated In Vascular Smooth Muscle Cell Calcification

Blood vessels calcification correlates with increased morbidity andmortality in patients suffering atherosclerosis, diabetes, and end-stage kidneydisease. Promoted inflammasome activation has been shown to take patr inthe pathogenesis of atherosclerosis. Meanwhile, the role of inflammasomeactivation on the development of vascular calcification has not beeninvestigated.β-Glycerophosphate β-GP) was used as a procedure to induce extensiveartery calcification in primary vascular smooth muscle cells (VSMCs). Analysisof the levels of NALP3inflammasome complex was performed by westernblotting, cell staining and mouse model. The effect of NALP3deficiency onVSMC calcification was examined after transfecting NALP3siRNA intocultured VSMCs.This essay demonstrated that the expression levels of NALP3inflammasome complex including NALP3and Caspase-1were enhanced incalcifying VSMCs, resulting in developed IL-1β secretion. Inhibition ofinflammasome activation by NALP3RNA interference reduced IL-1β secretionand inhibited VSMC calcification. Further analysis of mouse model specimensindicated that NALP3inflammasome was tightly correlated with arterialcalcification disease.My findings indicated that activation of the NALP3-mediated inflammatoryresponse pathway is a likely node associated with host response andpathogenesis of VSMC calcification, but to convince this association, morebiochemical and clinical tests are still needed.