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MicroRNA expression analysis following 24h siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells.

ABSTRACT: We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the microRNA expression in the human pulmonary arterial smooth muscle cells (hPASMC), at 24h timepoint.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92554 | GEO | 2017/12/16

SECONDARY ACCESSION(S): PRJNA358032

REPOSITORIES: GEO

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Gene expression analysis following 24h- and 48h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

Project description:We explored the impact of siRNA-mediated knockdown of the transforming growth factor β receptor III (TGFBR3) on the gene expression in the human pulmonary arterial smooth muscle cells (hPASMC), at 24h and 48h.

2017-12-15 | GSE92481 | GEO

Gene expression analysis following 6h-, 12h-, 18h- and 24h-siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells (hPASMC).

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Gene expression analysis following 24h siRNA-mediated knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial endothelial cells (hPAEC).

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Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

2014-02-06 | GSE54756 | GEO

Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures

Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system. Control (N=3) and TGFBR3KD (N=3) samples were hybridized to the Human gene 1.0 ST array, scanned with Affymetrix using AGCC v. 3.2.4 and then analyzed in R 3.0.1 using the oligo package.

2014-02-06 | E-GEOD-54756 | biostudies-arrayexpress

Decreased TGFBR3/Betaglycan expression enhances the metastatic abilities of renal cell carcinoma cells through TGF-b-dependent and independent mechanisms

Project description:It is unclear how the loss of TGF-b signaling components affects metastatic abilities in clear cell renal cell carcinoma (ccRCC). In this study, we identified that low TGFBR3 expression in ccRCC cells enhanced primary tumor formation and lung metastasis. In the presence of TGFBR3, TGF-b2 decreased the aldehyde dehydrogenase (ALDH)-positive ccRCC cell population, in which renal cancer-initiating cells are enriched. Loss of TGFBR3 also enhanced cell migration in cell culture and induced expression of several mesenchymal markers in a TGF-b-independent manner. Increased lamellipodium formation by FAK-PI3K signaling was observed with TGFBR3 downregulation, and this contributed to TGF-b-independent cell migration in ccRCC cells. Taken together, our findings reveal that loss of TGFBR3 endows ccRCC cells with multiple metastatic abilities through TGF-b-dependent and independent pathways.

2018-06-28 | GSE106719 | GEO

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (miRNA profiling)

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.

2014-01-22 | E-GEOD-42015 | biostudies-arrayexpress

Murine pulmonary arterial smooth muscle cells: Wild-type vs. NOX1 deficiency (mRNA profiling)

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 α-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. Transcriptional profiling of mouse pulmonary arterial smooth muscle cells in wild-type and NOX1-KO was analyzed. Pulmonary arterial smooth muscle cells were harvested from 3 mice.

2014-01-22 | E-GEOD-42014 | biostudies-arrayexpress

Genetic ablation of TonEBP/NFAT5 in smooth muscle cells inhibits arterial remodeling

Project description:Chronic biomechanical stress elicits remodeling of the arterial wall and causes detrimental arterial stenosis and stiffening. In this context, molecular determinants controlling proliferation and stress responses of vascular smooth muscle cells (VSMCs) have been insufficiently studied. We identified the transcription factor ‘nuclear factor of activated T-cells 5’ (NFAT5) as crucial regulatory element of mechanical stress responses of VSMCs. The relevance of this observation for biomechanically induced arterial remodeling was investigated in mice upon SMC-specific knockdown of NFAT5. While blood pressure levels, vascular architecture and flow-induced collateral growth were not affected in these mice, both hypertension-mediated arterial thickening and muscularization of pulmonary arteries during pulmonary artery hypertension (PAH) were impaired. In all models, a decrease in VSMC proliferation was observed indicating that NFAT5 controls activation of VSMCs in the remodeling arterial wall. Mechanistically, mechanoactivation of VSMCs promotes nuclear translocation NFTA5c upon its phosphorylation at Y143 and dephosphorylation at S1197. As evidenced by transcriptome studies, loss of NFAT5 in mechanoactivated VSMCs impairs expression of gene products controlling cell cycle and transcription/translation. These findings identify NFAT5 as molecular determinant of VSMC responses to biomechanical stress and arterial thickening.

2018-08-10 | GSE106274 | GEO

HDAC9 Complex Inhibition Improves Smooth Muscle Dependent Arterial Stenosis

Project description:Patients with heterozygous missense mutations in the ACTA2 or MYH11 genes are known to exhibit thoracic aortic aneurysm (TAA) and a risk of early onset aortic dissection. However, less common phenotypes involving arterial obstruction are also observed, including coronary and cerebrovascular stenotic disease. Recently an epigenetic complex containing the histone deacetylase HDAC9 and the long noncoding RNA, MALAT1 was implicated in pathologic vascular smooth muscle cell phenotypic changes in aneurysmal disease, however its involvement in stenotic disease has not been explored. Herein we implicate the HDAC9-MALAT1 complex in transcriptional silencing of contractile associated gene products, known to undergo downregulation in stenotic lesions. Furthermore, neointimal formation was inhibited in Hdac9 or Malat1 deficient mice with preservation of contractile protein expression. Pharmacologic targeting of the complex through either MALAT1 antisense oligonucleotides or inhibition of the methyltransferase EZH2 reduced neointimal formation. In conclusion, we report the implication of the HDAC9-MALAT1 complex in stenotic disease and demonstrate that pharmacologic therapy based on epigenetic targets can ameliorate arterial obstruction in an experimental system.

2021-09-01 | GSE120394 | GEO

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