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Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Robert Ivanek

PROVIDER: E-GEOD-82074 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Next Generation Sequencing of megakaryocyte-erythrocyte progenitor cells (MEPs) with or without mutations in JAK2 and Ezh2

Project description:Comparison of mRNA expression profiles of MEPs with or without mutations in JAK2 and Ezh2 by RNA sequencing. MEPs mRNA was extracted from six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) 10 weeks after tamoxifen injection. Our study represents the first detailed analysis of mRNA expression profile of MEP with or without mutations in JAK2 and Ezh2 , with biologic replicates, generated by RNA-seq technology. Our results revealed that mRNA expression profile of MEP with different genotype showed specific gene expression patterns, which allows to do biological comprehensive and quantitative analysis for hematopoiesis. MEPs mRNA profiles six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) were generated by deep sequencing.

2016-06-24 | E-GEOD-82072 | biostudies-arrayexpress

Next Generation Sequencing of long-term hematopoietic cells (LT-HSCs) with or without mutations in JAK2 and Ezh2

Project description:Comparison of mRNA expression profiles of LT-HSCs with or without mutations in JAK2 and Ezh2 by RNA sequencing. LT-HSC mRNA was extracted from six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) 10 weeks after tamoxifen injection. Our study represents the first detailed analysis of mRNA expression profile of LT-HSC with or without mutations in JAK2 and Ezh2 , with biologic replicates, generated by RNA-seq technology. Our results revealed that mRNA expression profile of LT-HSC with different genotype showed specific gene expression patterns, which allows to do biological comprehensive and quantitative analysis for hematopoiesis. LT-HSCs mRNA profiles six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) were generated by deep sequencing.

2016-06-24 | E-GEOD-82073 | biostudies-arrayexpress

Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis.

Project description: Not available

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Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-24 | GSE82074 | GEO

Chronic inflammation decreases HSC fitness via hyperactivation of the druggable IL-6/Jak/Stat3 signaling pathway.

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Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis

Project description:Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis

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Inhibition of Osteoblast Differentiation by JAK2<sup>V617F</sup> Megakaryocytes Derived From Male Mice With Primary Myelofibrosis.

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Results of a phase 2 study of pacritinib (SB1518), a JAK2/JAK2(V617F) inhibitor, in patients with myelofibrosis.

Project description: Not available

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Blood flow diverts extracellular vesicles from endothelial degradative compartments to promote angiogenesis

Project description:Extracellular vesicles released by tumors (tEVs) disseminate via circulatory networks and promote microenvironmental changes in distant organs favoring metastatic seeding. Despite their abundance in the bloodstream, how hemodynamics affect the function of circulating tEVs remains unsolved. We experimentally tuned flow profiles in vitro (microfluidics) and in vivo (zebrafish) and demonstrated that efficient uptake of tEVs occurs in endothelial cells subjected to capillary-like hemodynamics. Such flow profiles partially reroute internalized tEVs towards non-acidic and non-degradative Rab14-positive endosomes, at the expense of lysosomes, suggesting that endothelial mechanosensing diverts tEVs from degradation. Subsequently, tEVs promote the expression of pro-angiogenic transcription factors in flow-stimulated endothelial cells and favor vessel sprouting in zebrafish. Altogether, we demonstrate that capillary-like flow profiles potentiate the pro-tumoral function of circulating tEVs by promoting their uptake and rerouting their trafficking. We propose that tEVs contribute to pre-metastatic niche formation by exploiting endothelial mechanosensing in specific vascular regions with permissive hemodynamics. This set of experiments represents RNAseq of HUVEC cells subjected to 400 µm/s flow versus no flow (static conditon).

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