Project description:A number of mediators that have been found to be involved in the pathogenesis of hypoxic pulmonary hypertension, these mediators including mRNA, microRNAs and long noncoding RNAs. Endothelial dysfunction plays a major role in the initiation of pulmonary vascular remodeling and is thought to be a major contributor to this process. However, mRNA and no-coding RNAs expression profiles and their biological functions in pulmonary artery endothelial cells (PAECs) exposed to hypoxia need to be investigated further. Pulmonary artery endothelial cells (PAECs) were exposed to normoxia condition (21% O2, 5% CO2, 74% N2) or hypoxia condition (3% O2, 5% CO2, 92% N2) (n=3 for each group).PAECs were harvested after 24 hours and performed to further analysis.
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.
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:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison
Project description:In this study, we analzyed differences in the effect of hypoxia on the transcriptomic profile of cultured human pulmonary artery endothelial cells (HPAECs) vs. human brain microvascular endothelial cells (HBMVECs). To determine which hypoxia-regulated genes were dependent on hypoxia inducible factor 1-alpha (HIF-1alpha), some cells were transfected with an siRNA against HIF-1alpha prior to treatment with hypoxia. At the completion of the treatment protocol, mRNA was isolated using standard methodology and analyzed further by RNA-seq.
Project description:Intermittent hypoxia (IH) in HeLa cell culture activates proinflammatory transcription factor NFκB, whereas chronic hypoxia (CH) does not. In order to determine whether IH may be linked to vascular inflammation, we developed a novel IH cell culture system and exposed HAEC (human aortic endothelial cells) to IH or CH. Keywords: Human Artery Endothelial Cells (HAEC)
Project description:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison The response of each cell type (HAEC and HPAEC) to short-term chronic hypoxia was determined by a single SAGE library for each of three time points (0h, 8h and 24h)
Project description:To identify CLIC4 effectors by studying proteins expressiosn altered by CLIC4 overexpression in human pulmonary artery endothelial cells.
