A miRNA Cassette Reprograms Smooth Muscle Cells into Endothelial Cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA753869 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15417951_1.fastq.gz | Fastqsanger.gz | |||
| SRR15417951_2.fastq.gz | Fastqsanger.gz | |||
| SRR15417952_1.fastq.gz | Fastqsanger.gz | |||
| SRR15417952_2.fastq.gz | Fastqsanger.gz | |||
| SRR15417953_1.fastq.gz | Fastqsanger.gz |
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Project description:We report the differentially expressed genes in CASMCs, HUVECs, and induced EC (iECs).
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Project description:Objective: Vascular smooth muscle cells (VSMCs) undergo the phenotypic changes from contractile to synthetic state during vascular remodeling after ischemia. SIRT1 protects against stress-induced vascular remodeling via maintaining VSMC differentiated phenotype. However, the effect of smooth muscle SIRT1 on the functions of endothelial cells (ECs) has not been well clarified. Here, we explored the role of smooth muscle SIRT1 in endothelial angiogenesis after ischemia and the underlying mechanisms. Methods: We performed a femoral artery ligation model using VSMC specific human SIRT1 transgenic (SIRT1-Tg) and knockout (KO) mice. Angiogenesis was assessed in in vivo by quantification of the total number of capillaries, wound healing and matrigel plug assays, and in vitro ECs by tube formation, proliferation and migration assays. The interaction of HIF1? with circRNA was examined by using RNA immunoprecipitation, RNA pull-down and in situ hybridization assays. Results: The blood flow recovery was significantly attenuated in SIRT1-Tg mice, and markedly improved in SIRT1-Tg mice treated with SIRT1 inhibitor EX527 and in SIRT1-KO mice. The density of capillaries significantly decreased in the ischemic gastrocnemius of SIRT1-Tg mice compared with SIRT1-KO and WT mice, with reduced expression of VEGFA, which resulted in decreased number of arterioles. We identified that the phenotypic switching of SIRT1-Tg VSMCs was attenuated in response to hypoxia, with high levels of contractile proteins and reduced expression of the synthetic markers and NG2, compared with SIRT1-KO and WT VSMCs. Mechanistically, SIRT1-Tg VSMCs inhibited endothelial angiogenic activity induced by hypoxia via the exosome cZFP609. The cZFP609 was delivered into ECs, and detained HIF1? in the cytoplasm via its interaction with HIF1?, thereby inhibiting VEGFA expression and endothelial angiogenic functions. Meantime, the high cZFP609 expression was observed in the plasma of the patients with atherosclerotic or diabetic lower extremity peripheral artery disease, associated with reduced ankle-brachial index. Knockdown of cZFP609 improved blood flow recovery after hindlimb ischemia in SIRT1-Tg mice. Conclusions: Our findings demonstrate that SIRT1 may impair the plasticity of VSMCs. cZFP609 mediates VSMCs to reprogram endothelial functions, and serves as a valuable indicator to assess the prognosis and clinical outcomes of ischemic diseases.
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Project description:Thiele2013 - Smooth muscle smooth muscle cells
The model of smooth muscle smooth muscle cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110025
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110025 | BioModels
Project description:Integron gene cassette metagenome
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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.
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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
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Project description:Purpose: global gene expression profiling of H1 and iPSC derived endothelial cells (ECs) and smooth mucle cells (SMCs). Methods: SMART-seq2 amplified polyA RNA from undifferentiated H1 cells and iPSCs (in biological duplicates), cardiovascular progenitor cells, endothelial cells (ECs) and smooth muscle cells (SMCs) Results: Insulin free condition promoted cardiovascular mesoderm, endothelial and smooth muscle differentiation. Conclusions: the gene expression profiles of ECs and SMCs differentiated in insulin free medium confirmed that they are true ECs and SMCs.
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Project description:NOX1 is a catalytic subunit of nonphagocytic NADPH oxidase, mainly localized to smooth muscle cells in the vasculature. We investigated the pathology underlying the pulmonary arterial hypertension-like phenotype demonstrated in mice deficient in the Nox1 gene (Nox1-KO). Spontaneous enlargement and hypertrophy of the right ventricle, accompanied by hypertrophy of pulmonary vessels, were demonstrated in Nox1-KO at 9-18 weeks of age. Since an increased number of ?-smooth muscle actin-positive vessels was observed in Nox1-KO, pulmonary arterial smooth muscle cells (PASMCs) were isolated and characterized by flow cytometry and TUNEL staining. In Nox1-/Y PASMC, the number of apoptotic cells was significantly reduced without any change in the expression of endothelin-1, and hypoxia-inducible factors HIF-1a and HIF-2a, factors implicated in the pathogenesis of PAH. microRNA expression profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed. Pulmonary arterial smooth muscle cells were harvested form 3 mice.
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