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Transforming Growth Factor-β (TGFβ) Prevents Hypertensive Aortic Dissection in Adult Mice via Extracellular Matrix Production (Bulk KO vs. WT Aorta)

ABSTRACT: Transforming Growth Factor-β (TGFβ) Prevents Hypertensive Aortic Dissection in Adult Mice via Extracellular Matrix Production (Bulk KO vs. WT Aorta)

PROVIDER: PRJNA799022 | ENA |

REPOSITORIES: ENA

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Transforming growth factor beta signaling in hypertensive remodeling of porcine aorta

Project description:A porcine aortic coarctation model was used to examine regulation of gene expression in early hypertensive vascular remodeling. Aortic segments were collected proximal (high pressure) and distal (low pressure) to the coarctation after 2 weeks of sustained hypertension (mean arterial pressure>150mmHg). Porcine 10K oligoarrays used for gene expression profiling of the two regions of aorta revealed downregulation of cytoskeletal and upregulation of extracellular region genes relative to the whole genome. A genomic database search for transforming growth factor-β (TGFβ) control elements (TCE) showed that 19% of the genes that changed expression due to hypertension contained putative TCEs. Real time PCR and microarray analysis showed no change in expression of TGFβ1, TGFβ2, TGFβ3, or bone morphogenetc proteins (BMP)2 and 4, yet immunohistochemical staining for phosphorylated SMAD2, an indicator of TGFβ signaling, and for phosphorylated SMAD1/5/8, an indicator of signaling through the BMPs, showed the highest percentage of positively stained cells in the proximal aortic segments of occluded animals. For TGFβ signaling, this increase was significantly different from sham-operated controls. Western blot analysis showed no difference in total TGFβ1 protein levels with respect to treatment or aortic segment. Immunohistochemistry showed that the protein levels of latency associated peptide, was decreased in proximal segments of occluded animals. Collectively, these results suggest that activation of TGFβ, but not altered expression, may be a major mechanism regulating early hypertensive vascular remodeling.

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Transforming Growth Factor-β (TGFβ) Prevents Hypertensive Aortic Dissection in Adult Mice via Extracellular Matrix Production (Bulk KO vs. WT Aorta)

Project description:We report bulk RNA-seq data of murine aortas at 1 week after conditional disruption of TGFβ signaling in SMCs versus controls

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Transforming Growth Factor-β (TGFβ) Prevents Hypertension-Induced Aortic Dissection in Adult Mice via Extracellular Matrix Production (single cells WT Aorta)

Project description:Transforming Growth Factor-β (TGFβ) Prevents Hypertension-Induced Aortic Dissection in Adult Mice via Extracellular Matrix Production (single cells WT Aorta)

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Project description:Glioblastoma stem cells (GSCs) fate is controlled by environmental cues, among which cytokines play a crucial role. The transforming growth factor β (TGFβ) family signaling pathways controls GSCs. On one hand, TGFβ promotes cell proliferation in GBM, it induces the expression of platelet-derived growth factor-B (PDGFB). Moreover, TGFβ, via its signaling mediators Smad2/3, induces the expression of the cytokine leukemia inhibitory factor (LIF) and Sox4, which in turn enhances the expression of the stem cell transcription factor Sox2; this increases the self-renewal capacity of the GSCs and their stemness characteristics, and enhances the GSC tumor-initiating potential. On the other hand, Bone morphogenic proteins (BMPs) are known to promote GSC differentiation towards the astrocytic phenotype. To further understand which genes are regulated by TGFβ and BMP7 in GSCs we performed a microarray in the Affymetrix HTA2 platform in three different glioblastoma cell line, U2987, and two patient-derived glioblastoma stem cells, U3031MG and U3034MG, in the presence or absence of 5 ng/ml of TGFβ or 30 ng/ml BMP7 for 24 h, three biological replicates per condition.

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Transforming Growth Factor-β (TGFβ) Prevents Hypertension-Induced Aortic Dissection in Adult Mice via Extracellular Matrix Production

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