ABSTRACT: 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.
Project description:We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the gene expression in the human pulmonary arterial smooth muscle cells (hPASMC), following 6h, 12h, 18h and 24h.
Project description: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.
Project description:microRNA expression analysis following 24h siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells.
Project description:We explored the impact of transforming growth factor β receptor III (TGFBR3) knockdown on the gene expression in the human pulmonary arterial endothelial cells (hPASMC).
Project description: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).
Project description:Gene expression analysis following 24h siRNA-mediated knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial endothelial cells (hPAEC).
Project description:We aimed to identify the response mechanism to EGFR tyrosine kinase inhibition. A431 cells were transfected with mock siRNA or BCL6 siRNA. Cells were then treated with gefitinib. Harvesting was done at 0h, at 24h and at 48h. Two TMT10plex sets were organized as follows: TMT set1: mock 0h (3x, channels 126, 127N and 127C), mock 24h (3x, 128N, 128C and 129N), mock 48h (3x, 129C, 130N, 130C) and internal pooled standard (131) composed from equal aliquots of all samples (mock siRNA and BCL6 siRNA). TMT set2: siBCL6 0h (3x, channels 126, 127N and 127C), siBCL6 24h (3x, 128N, 128C and 129N), siBCL6 48h (3x, 129C, 130N, 130C) and the same internal pooled standard (131) as for set 1.
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.
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.
