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Endothelial Raf1 activation regulates arterial morphogenesis

ABSTRACT: Analyze effect of Raf1 S259A on gene expression in HUVEC

ORGANISM(S): Homo sapiens

PROVIDER: GSE42964 | GEO | 2012/12/18

SECONDARY ACCESSION(S): PRJNA183951

REPOSITORIES: GEO

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Endothelial Raf1 activation regulates arterial morphogenesis

Project description:Analyze effect of Raf1 S259A on gene expression in HUVEC Total RNA obtained from HUVEC infected with empty lentiviral vector pLVX-IRES-puro (control) or that expressing human RAF1 WT (WT) or RAF1 S259A (S259A).

2012-12-18 | E-GEOD-42964 | biostudies-arrayexpress

Endothelial RAF1/ERK activation regulates arterial morphogenesis.

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Gene expression data from MCF7 cells overexpressing RAF1

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Arterial-Venous Endothelial Cell Cycle Proteins Differential Expression

Project description:HUVEC-FUCCI cells were used to demonstrate that different endothelial cell cycle states provide distict windows of opportunity for gene expression in response to extrinsic signals. HUVEC-FUCCI were FACS-isolated into three different cell cycle states. Peptide digests from the resulting lysates showed differentially expressed proteins among the three cell cycles. These studies show that endothelial cell cycle state determines the propensity for arterial vs. venous fate specification.

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Cellular Interplay and Cytokine Hierarchy Cause Pathological Cardiac Hypertrophy in RAF1-Mutant Noonan Syndrome

Project description:Noonan syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofacial, growth, cognitive and cardiac defects. NS patients with kinase-activating RAF1 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1 L613V/+ knock-in mice. Here, using inducible Raf1 L613V expression, we show that LVH results from the interplay of cardiac cell types. Cardiomyocyte Raf1 L613V enhances Ca 2+ sensitivity and cardiac contractility without causing hypertrophy. Raf1 L613V expression in cardiomyocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis. Endothelial/endocardial (EC) Raf1 L613V causes cardiac hypertrophy without affecting contractility. Co-culture and neutralizing antibody experiments reveal a cytokine hierarchy (TNFα->IL6) from Raf1 L613V -expressing ECs that drives cardiomyocyte hypertrophy in vitro. Furthermore, post-natal TNFα inhibition normalizes the increased wall thickness and cardiomyocyte hypertrophy in vivo. We conclude that NS cardiomyopathy involves cardiomyocytes, ECs, and fibroblasts, TNFα/IL6 signaling components represent potential therapeutic targets, and abnormal EC signaling might contribute to other forms of LVH.

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Interactome dynamics of RAF1-BRAF kinase monomers and dimers

Project description:RAF kinases play major roles in cancer. BRAFV600E mutants drive ~6% of human cancers. Potent kinase inhibitors exist but show variable effects in different cancer types, sometimes even inducing paradoxical RAF kinase activation. Both paradoxical activation and drug resistance are frequently due to enhanced dimerization between RAF1 and BRAF, which maintains or restores the activity of the downstream MEK-ERK pathway. Here, using quantitative proteomics we mapped the interactomes of RAF1 monomers, RAF1-BRAF and RAF1-BRAFV600E dimers identifying and quantifying >1,000 proteins. In addition, we examined the effects of vemurafenib and sorafenib, two different types of clinically used RAF inhibitors. Using regression analysis to compare different conditions we found a large overlapping core interactome but also distinct condition specific differences. Given that RAF proteins have kinase independent functions such dynamic interactome changes could contribute to their functional diversification. Analysing this dataset may provide a deeper understanding of RAF signalling and mechanisms of resistance to RAF inhibitors.

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Project description:Gene expression profiles during the differentiation of HUVEC on matrigel were analyzed.

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Gene expression analysis during morphogenesis of Human umbilical vein endothelial cells

Project description:Gene expression profiles during the differentiation of HUVEC on matrigel were analyzed. RNA was isolated from Human umbilical vein endothelial cell during morphogenesis. HG-U133 plus 2.0 microarray (54675 human genes; Affymetrix Santa Clara, CA, USA) was performed.

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