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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).

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92481 | GEO | 2017/12/15

SECONDARY ACCESSION(S): PRJNA357647

REPOSITORIES: GEO

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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).

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).

2017-12-16 | GSE92553 | GEO

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 microRNA expression in the human pulmonary arterial smooth muscle cells (hPASMC), at 24h timepoint.

2017-12-16 | GSE92554 | 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).

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.

2017-12-15 | GSE92435 | GEO

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

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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

TGFBR3 inhibits the aggressive of papillary thyroid cancer by inhibiting PI3K/AKT pathway and EMT

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.

2024-05-18 | GSE265794 | GEO

Homo sapiens

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).

| PRJNA357647 | ENA

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

3'mRNA sequencing of hepatic RNA (MACE) at the time points 24h/48h after acetaminophen (APAP) (300mg/kg) administration

Project description:Hepatic RNA specimens from mice (C57BL/6) of the 4 groups (vehicle-treated at 24h/48h, n=6; acetaminophen (APAP)-treated (300mg/kg) at 24h/48h, n=7) were pooled at equal shares. Thereafter, pooled RNA underwent analysis by 3'mRNA sequencing (MACE, GenXPro, Frankurt, Germany).

2021-12-31 | GSE169071 | GEO

Transforming Growth Factor Beta Receptor 3 (TGFBR3)-Associated Membranous Nephropathy.

Project description:BackgroundMembranous lupus nephritis (MLN) comprises 10%-15% of lupus nephritis and increases morbidity and mortality of patients with SLE through complications of nephrotic syndrome and chronic kidney failure. Identification of the target antigens in MLN may enable noninvasive monitoring of disease activity, inform treatment decisions, and aid in prognostication, as is now possible for idiopathic MN caused by antibodies against the phospholipase A2 receptor. Here, we show evidence for type III TGF-β receptor (TGFBR3) as a novel biomarker expressed in a subset of patients with MLN.MethodsMass spectrometry was used for protein discovery through enrichment of glomerular proteins by laser capture microdissection and through elution of immune complexes within MLN biopsy specimens. Colocalization with IgG within glomerular immune deposits from patients and disease controls was evaluated by confocal microscopy. Immunostaining of consecutive case series was used to determine the overall frequency in MN and MLN.ResultsTGFBR3 was found to be enriched in glomeruli and coimmunoprecipitated with IgG within a subset of MLN biopsy specimens by mass spectrometry. Staining of consecutive MN cases without clinical evidence of SLE did not show TGFBR3 expression (zero of 104), but showed a 6% prevalence in MLN (11 of 199 cases). TGFBR3 colocalized with IgG along the glomerular basement membranes in TGFBR3-associated MN, but not in controls.ConclusionsPositive staining for TGFBR3 within glomerular immune deposits represents a distinct form of MN, substantially enriched in MLN. A diagnosis of TGFBR3-associated MN can alert the clinician to search for an underlying autoimmune disease.

| S-EPMC8676385 | biostudies-literature

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