Project description:Early transcriptomic response to n-LDL and ox-LDL in human vascular smooth muscle cells (hVSMC). We used microarrays with the aim of assessing early molecular changes that induce a response in the VSMC using native and oxidized low-density lipoprotein (n-LDL and ox-LDL).
Project description:Early transcriptomic response to n-LDL and ox-LDL in human vascular smooth muscle cells (hVSMC). We used microarrays with the aim of assessing early molecular changes that induce a response in the VSMC using native and oxidized low-density lipoprotein (n-LDL and ox-LDL). For each LDL internalization experiment, three biological replicates were used and the samples pooled with the aim of obtain three technical replicates (three arrays for condition).
Project description:Atherosclerosis (AT) is a chronic inflammatory disease characterized by the accumulation of inflammatory cells, lipoproteins and fibrous tissue in the walls of arteries. AT is the primary cause of heart attacks and stroke and the leading cause of death in westernized countries. To date, the pathogenesis of AT is not well-defined. Studies have shown that the dedifferentiation of contractile and quiescent vascular smooth muscle cells (SMC) to the proliferative, migratory and synthetic phenotype in the intima is pivotal for the onset and progression of AT. To further delineate the mechanisms underlying the pathogenesis of AT, we have analyzed the early molecular pathways and networks of SMC phenotype transformation as induced by the presence of minimally-oxidized LDL (moxLDL). 3 pooled samples were analyzed, one untreated control, one 3h after treatment, one 21h after treatment, no replicates
Project description:Atherosclerosis (AT) is a chronic inflammatory disease characterized by the accumulation of inflammatory cells, lipoproteins and fibrous tissue in the walls of arteries. AT is the primary cause of heart attacks and stroke and the leading cause of death in westernized countries. To date, the pathogenesis of AT is not well-defined. Studies have shown that the dedifferentiation of contractile and quiescent vascular smooth muscle cells (SMC) to the proliferative, migratory and synthetic phenotype in the intima is pivotal for the onset and progression of AT. To further delineate the mechanisms underlying the pathogenesis of AT, we have analyzed the early molecular pathways and networks of SMC phenotype transformation as induced by the presence of minimally-oxidized LDL (moxLDL).
Project description:Recent studies highlight the importance of lipotoxic damage in aortic cells as the major pathogenetic contributor of atherosclerotic disease. Since the STE20-type kinase STK25 has been shown to exacerbate ectopic lipid storage and associated cell injury in several metabolic organs, we here investigated its role in the main cell types of vasculature. We depleted STK25 by small interfering RNA in human aortic endothelial and smooth muscle cells exposed to oleic acid and oxidized LDL. In both cell types, the silencing of STK25 reduced lipid accumulation and suppressed activation of inflammatory and fibrotic pathways as well as lowered oxidative and endoplasmic reticulum stress. Notably, in smooth muscle cells, STK25 inactivation hindered the shift from a contractile to a synthetic phenotype. Together, we provide the first evidence that antagonizing STK25 signaling in human aortic endothelial and smooth muscle cells is atheroprotective, highlighting this kinase as a new potential therapeutic target for atherosclerotic disease.
Project description:Analysis of hypoxia-exposed human pulmonary artery smooth muscle cells to identify the commonly regulated genes by hypoxia. Results provide insight into the regulatory mechanism of hypoxic responses in vascular smooth muscle cells.
Project description:Analysis of hypoxia-exposed human pulmonary artery smooth muscle cells to identify the commonly regulated microRNAs by hypoxia. Results provide insight into the regulatory mechanism of hypoxic responses in vascular smooth muscle cells.
2019-09-25 | GSE118361 | GEO
Project description:RNA Seq of ox-LDL treated vascular smooth muscle cells
Project description:Mechanical stress plays important roles in vascular physiology and pathophysiology. Although vascular smooth muscle cells are continuously exposed to cyclic stretch and hydrostatic pressure, the individual effects of these mechanical stimuli on global molecular profiles remain poorly understood. Using a custom-made cyclic hydrostatic pressure culture system developed in our laboratory, we performed transcriptome analyses of human aortic smooth muscle cells exposed to cyclic stretch or hydrostatic pressure to characterize the molecular profiles induced by these stimuli.
