ABSTRACT: 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 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: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:microRNA expression analysis following 24h siRNA knockdown of transforming growth factor β receptor III (TGFBR3) in human pulmonary arterial smooth muscle cells.
Project description: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: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:CAV1 loss-of-function mutations have been associated with the development of pulmonary arterial hypertension (PAH). CAV1 is an integral component of endothelial caveolae, specialized lipid rafts that attach to the actin cytoskeleton and modulate receptor/signal transduction coupling. CAV1 loss in pulmonary artery endothelial cells produced a proliferative, hypermigratory cellular phenotype with a disrupted cytoskeletal architecture, mirroring known features of PAH pathobiology. Gene expression on Human Pulmonary Arterial Endothelial Cells (PAECs) transfected with non-targeting siRNA control pool or siRNA (ON-TARGET plus CAV1) in the presence or absence of TNF-alpha was evaluated
Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a proliferative endothelial cell phenotype, inflammation and pulmonary vascular remodeling. BMPR2 loss-of-function has been linked to pathologic plexiform lesions with obliteration of distal pulmonary arteries distal pulmonary arteries BMPR2 silencing inprimary human pulmonary artery ECs (HPAECs) recapitulate important aspects of cellular dysfunction and deregulated signaling associated with PAH. Primary HPAECs were transfected with gene-specific siRNA pools targeting BMPR2 or control siRNA followed PMA or control stimulation.
Project description:Transforming Growth Factor Beta Receptor III (TGFBR3) had been shown to play a tumor suppressor role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains a mystery. The purpose of this study was to determine the molecular mechanism and biological behavior of TGFBR3 in PTC, to further explore the regulatory pathway involved in TGFBR3 on PTC and provide potential targets for the diagnosis and treatment of invasive PTC.
