Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731342 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14598290_1.fastq.gz | Fastqsanger.gz | |||
| SRR14598290_2.fastq.gz | Fastqsanger.gz | |||
| SRR14598291_1.fastq.gz | Fastqsanger.gz | |||
| SRR14598291_2.fastq.gz | Fastqsanger.gz | |||
| SRR14598292_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
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: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: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:Aortic smooth muscle cell (SMC) phenotype modulation is a central feature of cell-mediated pathology in Marfan syndrome aortic aneurysm and Klf4 is proposed to contribute to this process. We generated mice with smooth muscle cell-specific Klf4 deletion using an Myh11-creERT2 transgene, induced deletion at 8 weeks and performed single cell RNA sequencing at 24 weeks on whole aortic root tissues.
2022-08-23 | GSE206227 | GEO
Project description:Smooth muscle cell (SMC) loss is the characteristic feature in the pathogenesis of aortic dissection (AD), and ferroptosis is a novel iron-dependent regulated cell death driven by the excessive lipid peroxidation accumula_x0002_tion. However, whether targeting ferroptosis is an effective approach for SMC loss and AD treatment remains unclear. Here, we found that the iron level, ferroptosis-related molecules TFR, HOMX1, ferritin and the lipid peroxidation product 4-hydroxynonenal were increased in the aorta of AD. Then, we screened several inhibitors of histone methyltransferases and found that BRD4770 had a protective effect on cystine deprivation-, imidazole ketone erastin- or RSL3-induced ferroptosis of SMCs. The classic ferroptosis pathways, System Xc--GPX4, FSP1- CoQ10 and GCH1-BH4 pathways which were inhibited by ferroptosis inducers, were re-activated by BRD4770 via inhibiting mono-, di- and tri- methylated histone H3 at lysine 9 (H3K9me1/2/3). RNA-sequencing analysis revealed that there was a positive feedback regulation between ferroptosis and inflammatory response, and BRD4770 can reverse the effects of inflammation activation on ferroptosis. More importantly, treatment with BRD4770 attenuated aortic dilation and decreased morbidity and mortality in a β-Aminopropionitrile monofumarate-induced mouse AD model via inhibiting the inflammatory response, lipid peroxidation and fer_x0002_roptosis. Taken together, our findings demonstrate that ferroptosis is a novel and critical pathological mechanism that is involved in SMC loss and AD development. BRD4770 is a novel ferroptosis inhibitor and has equivalent protective effect to Ferrostatin-1 at the optimal concentration. Translating insights into the anti-ferroptosis ef_x0002_fects of BRD4770 may reveal a potential therapeutic approach for targeting SMC ferroptosis in AD.
2024-07-16 | GSE272018 | 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