Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731342 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To study the impact of the transcription factor NFAT5 on the vascular smooth muscle cell (VSMC) transcriptome, genetic ablation of floxed nfat5 in mouse aortic smooth muscle cells was achieved by transducing them with an adenoviral vector to express Cre-recombinase (Ad-Cre) under control of a CMV promoter. Empty vector adenovirus (Ad-PL) was used as control.
2018-10-10 | GSE109864 | GEO
Project description:Derivation of induced smooth muscle cells (iSMC) through direct transdifferentiation of a convenient and expandable primary cell source would open a wide range of prospects for their use in tissue engineering, drug testing, and disease modeling. Hypothesizing that MYOCD as a master regulator of smooth muscle gene expression would facilitate the generation of iSMC, we studied the conversion of human endothelial progenitor cells (EPC) into iSMC through the induced expression of by over-expression of MYOCD. A significant cytoskeletal rearrangement of the EPC resembling that of mesenchymal cells occurred within 3 days post initiation of MYOCD expression. This transition was associated with a downregulation of endothelial cell surface markers (CD31, CD105) as determined by flow cytometry. By day 7, iSMC derivation was evident with a significant upregulation of smooth muscle markers ACTA2, MYH11, TAGLN, and downregulation of CD31 and CDH5 as determined by gene expression analysis. Immunofluorescence revealed expression of MYH11 and ACTA2 and absence of endothelial markers VWF and CD31. By two weeks, microarray gene expression analysis demonstrated a significant similarity between iSMC and umbilical artery SMC (UASMC). The iSMC continued to develop toward the SMC lineage after four weeks of MYOCD induced expression. Microarray gene expression analysis showed an upregulation of molecular pathways associated with smooth muscle contraction and cytoskeletal reorganization in iSMC. Calcium transients were detected in iSMC when stimulated with phenylephrine but not in EPC. Contractility of iSMC was also higher than that of EPC as determined by traction force microscopy. Tissue-engineered blood vessels constructed using iSMC showed functionality with respect to flow- and drug- mediated vasodilation and vasoconstriction. We used microarrays to detail the global programme of gene expression underlying the transdifferentiation of endothelial progenitor cells into smooth muscle cells via the transient induced expression of the transcriptional co factor MYOCD
2016-03-21 | GSE73469 | GEO
Project description:In the urinary tract, smooth muscle (SM) is present in the renal pelvis, the ureter, the bladder and the urethra and plays a crucial role in the functional and structural integrity of these organs. In Tshz3 mutant ureters the myogenic program is not activated in the proximal region due to the absence of expression of myocardin (Myocd), a key regulator of SM differentiation. We set out to characterize TSHZ3-dependent mechanisms that participate to the process of ureteric smooth muscle cells (SMC) differentiation. To this aim, we used microarrays to identify distinct classes of up- and down-regulated genes in Tshz3LAcZ/LacZ mutant ureters at two different time points; at E14.5, which corresponds to the onset of the myogenic program and at E16.5, when SMC express the full repertoire of differentiation marker genes. Mouse embryonic (E14.5 and E16.5) wild type and Tshz3LacZ/LacZ mutant ureters were dissected for RNA extraction and hybridization on Affymetrix microarrays.
2013-02-01 | E-GEOD-43940 | biostudies-arrayexpress
Project description:Vascular smooth muscle cell plasticity plays a pivotal role in the pathophysiology of vascular diseases. Despite compelling evidence demonstrating the importance of transcription factor GATA6 in vascular smooth muscle, the functional role of GATA6 remains poorly understood. The aim of this study was to elucidate the role of GATA6 on cell migration and to gain insight into GATA6-sensitive genes in smooth muscle. Therefore, we performed Affymetrix microarray analysis on human coronary artery smooth muscle cells after overexpressing GATA6 by adenovirus transduction and compared it to control which are cell transduced with Ad-CMV-null.
2022-10-31 | GSE216686 | GEO
Project description:In the urinary tract, smooth muscle (SM) is present in the renal pelvis, the ureter, the bladder and the urethra and plays a crucial role in the functional and structural integrity of these organs. In Tshz3 mutant ureters the myogenic program is not activated in the proximal region due to the absence of expression of myocardin (Myocd), a key regulator of SM differentiation. We set out to characterize TSHZ3-dependent mechanisms that participate to the process of ureteric smooth muscle cells (SMC) differentiation. To this aim, we used microarrays to identify distinct classes of up- and down-regulated genes in Tshz3LAcZ/LacZ mutant ureters at two different time points; at E14.5, which corresponds to the onset of the myogenic program and at E16.5, when SMC express the full repertoire of differentiation marker genes.
2013-02-01 | GSE43940 | GEO
Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic miRNA to examine the effect of age on vascular miRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33 Total miRNA was extracted from young (3-4 mo) and aged male (12mo) MR-intact and SMC-MR-KO mice to investigate aging-induced alterations in vascular miRNA expression
2016-07-29 | E-GEOD-84960 | biostudies-arrayexpress
Project description:To identify novel genes especially lncRNAs linked to vascular smooth muscle cell (VSMC) differentiation, we performed RNA sequencing of adenovirus–MYOCD transduced human coronary artery smooth muscle cells (HCASMs). Simiilar amount of empty Adenovirus was used as control.
2016-08-31 | GSE77120 | GEO
Project description:To investigate the role of TET2 in osteogenic differentiation of smooth muscle cells (SMCs) in vivo, we performed single cell RNA-seq in cholecalciferol overload-induced calcified aortas of Tet2flox/flox and SMC specific Tet2 knock-out mice (Tet2SMC-KO).
2024-04-16 | GSE263739 | GEO
Project description:LncRNA and mRNA expression profiles in aortic smooth muscle cells with Srf knockout or Myocd over-expression were analyzed by Arraystar Mouse LncRNA Microarray V3.0.
2017-03-08 | GSE85930 | GEO
Project description:Tissue Factor Pathway Inhibitor-2 is Induced by Fluid Shear Stress in Vascular Smooth Muscle Cells and Affects Cell Proliferation and Survival Introduction: Vascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. Here, we investigated the effect of FSS on SMC gene expression and function. Methods: Laminar FSS of arterial level (14 dynes/cm2) was applied to SMC cultures for 24 h in a parallel-plate flow chamber. The effect of FSS on gene expression was first screened with microarray technology and the results further verified by real time (RT) PCR and immunoblotting. Protein expression was also studied in the rat carotid artery after balloon-injury and DNA synthesis and apoptosis was examined in SMCs in vitro. Results: Microarrays identified tissue-pathway inhibitor-2 (TFPI-2) as the most differentially expressed gene by FSS in cultured SMCs. The regulatory effect of FSS on the expression of TFPI-2 was confirmed by RT-PCR and immunobloting demonstrating a more than 400-fold increase in TFPI-2 expression in SMCs exposed to FSS compared to static controls and a consistent upregulation at the protein level. Functionally, SMC proliferation was decreased by FSS and recombinant TFPI-2 was found to inhibit SMC proliferation and induce SMC apoptosis as indicated by activation of caspase-3. In vivo, TFPI-2 expression was found to be up-regulated 5, 10 and 20 h after rat carotid balloon-injury and immunohistochemistry demonstrated TFPI-2 protein in luminal SMCs exposed to FSS in rat carotid intimal hyperplasia 10 days after balloon-injury. Conclusion: FSS strongly influence gene expression in cultured SMCs and induce TFPI-2 expression, which is also expressed after rat carotid balloon injury in luminal SMCs exposed to FSS. Functionally, TFPI-2 may play an important role in vessel wall repair by regulating SMC proliferation and survival. Further studies are needed to elucidate the mechanisms by which TFPI-2 control SMC function. 3 x 2 samples from a paired fluid shear stress experiment on smooth muscle cells.
2010-04-12 | E-GEOD-19909 | biostudies-arrayexpress