Project description:Transcriptomics analysis of human coronary artery smooth muscle cells cultured in osteogenic medium and PIKfyve inhibition. To study the underlying molecular mechanisms of PIKfyve-mediated vascular calcification, we analyzed the transcriptome of osteogenic medium (OM)-calcified human coronary artery smooth muscle cells that were treated with PIKfyve inhibitors (Apilimod, YM201636) or DMSO control on day 7.
Project description:Smooth muscle cells retain a high plasticity in adulthood, allowing them to change between a differentiated, contractile phenotype and a dedifferentiated, proliferative and migrative phenotype in response to microenvironmental cues. This plasticity is key to maintain the structure and function of vessel walls. When disregulated, it can lead to the onset of vascular pathologies related to vascular remodeling and excessive extracellular matrix deposition. This screening aims to find novel candidates involved in the regulation of this process, in particular long non-coding RNAs (lncRNAs).
Project description:Transcriptomics analysis of human coronary artery smooth muscle cells cultured in osteogenic medium (OM) to induce a mineralized extracellular matrix. To study the underlying molecular mechanisms driving vascular calcification, we analyzed the transcriptome of osteogenic medium (OM)-calcified human coronary artery smooth muscle cells on day 7.
Project description:The phenotypes of endothelial cells (ECs) in conduit and resistance arteries differ in part due to the presence of myoendothelial junctions in resistance arteries. These are direct contact points between ECs and smooth muscle cells (SMCs) that form through holes in the inner elastic lamina. To investigate the consequences of SCM contact on endothelial phenotypes, we used transwells to culture ECs in three conditions: cultured without SMCs (monolayer ECs), co-cultured without direct contact with SMCs (no-contact ECs), and co-cultured with SMCs such that myoendothelial junctions could form (contact ECs). We then collected the ECs and performed bulk RNA sequencing. These data demonstrate the impact of SMC-derived signals on endothelial phenotypes.
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:CSHL Long RNA Seq HPASMC cell total (SID38228, SID38229) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:Excessive TGF-β signalling has been shown to underlie pulmonary hypertension (PAH). Human pulmonary artery smooth muscle cells (HPASMCs) can release extracellular vesicles (EVs) but their content and significance have not yet been studied. Here, we analysed the content and biological relevance of HPASMC-derived EVs. We used low-input RNA-Seq to analyse the RNAs of EVs released by HPASMC under basal conditions. This data was compared to cellular RNAs. The same experiments (RNA-seq of EV and cellular RNAs) were carried out on HPASMC treated with TGF-b1 and BMP4, recapitulating pathological conditions.