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Effect of Hairy and Enhancer of Split 1 (HES1) activation on gene expression of mature osteoclasts

ABSTRACT: Effect of Hairy and Enhancer of Split 1 (HES1) activation on gene expression of mature osteoclasts

PROVIDER: PRJNA853757 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19886866_1.fastq.gz	Fastqsanger.gz
	SRR19886866_2.fastq.gz	Fastqsanger.gz
	SRR19886867_1.fastq.gz	Fastqsanger.gz
	SRR19886867_2.fastq.gz	Fastqsanger.gz
	SRR19886868_1.fastq.gz	Fastqsanger.gz

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Effect of Hairy and Enhancer of Split 1 (HES1) activation on gene expression of mature osteoclasts

Project description:To investigate the role of HES1 in osteoclast differentiation and function, bone marrow-derived macrophages (BMMs) were derived from CtskCre/WT;RosaHes1 and control (Rosa[STOP]Hes1 ) mice and were differentiated into mature osteoclasts. We then performed gene expression profiling analysis using data obtained from RNA-seq of conrol and HES1-overexpressing osteoclasts.

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Hes1 is responsible for Notch signaling-mediated suppression of acute myeloid leukemia development

Project description:In leukemogenesis Notch signaling can be up- and down-regulated in a context-dependent manner. Here we report that deletion of hairy and enhancer of split-1 (Hes1) promotes acute myeloid leukemia (AML) development induced by the MLL-AF9 fusion protein. Subsequently, the FMS-like tyrosine kinase 3 (FLT3) was up-regulated in mouse cells of a Hes1- or RBP-J-null background. MLL-AF9-expressing Hes1-null AML cells showed enhanced proliferation and ERK phosphorylation following FLT3 ligand stimulation. FLT3 inhibition efficiently abrogated proliferation of MLL-AF9-induced Hes1-null AML cells. Furthermore, an agonistic anti-Notch2 antibody induced apoptosis of MLL-AF9-induced AML cells in a Hes1-wild type but not a Hes1-null background. These observations demonstrate that Hes1 mediates tumor suppressive roles of Notch signaling in AML development by down-regulating FLT3 expression.

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Project description:Inflammatory bone destruction was induced by locally injecting lipopolysaccharides into fluorescent reporter mice of mature osteoclasts or their precursors. These mice were treated with a JAK inhibitor, ABT-317, which selectively inhibits the activation of JAK1, and intravital imaging with multiphoton microscopy was conducted. We also investigated the molecular mechanism of the effects of the JAK inhibitor on osteoclasts by exhaustive RNA sequence analysis.

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Project description:Notch signaling plays both oncogenic and tumor suppressor roles, depending on cell type. In contrast to T cell acute lymphoblastic leukemia (T-ALL), where Notch activation promotes leukemogenesis, induction of Notch signaling in B-ALL leads to growth arrest and apoptosis. The Notch target Hairy/Enhancer of Split1 (HES1) is sufficient to reproduce this tumor suppressor phenotype in B-ALL, however the mechanism is not yet known. Here we report that HES1 regulates pro-apoptotic signals via the novel interacting protein Poly ADP-Ribose Polymerase1 (PARP1) in a cell type-specific manner. The interaction of HES1 with PARP1 inhibits HES1 function, induces PARP1 activation and results in PARP1 cleavage in B-ALL. HES1-induced PARP1 activation leads to self-ADP ribosylation of PARP1, consumption of NAD+, diminished ATP levels, and translocation of the Apoptosis Inducing Factor (AIF) from mitochondria to the nucleus, resulting in apoptosis in B-ALL, but not T-ALL. Importantly, induction of Notch signaling via the Notch agonist peptide DSL can reproduce these events and leads to BALL apoptosis. The novel interaction of HES1 and PARP1 in B-ALL modulates the function of the HES1 transcriptional complex and signals through PARP1 to induce apoptosis. This mechanism reveals a cell type-specific pro-apoptotic pathway which may lead to Notch agonist-based cancer therapeutics.

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Gene expression alteration in chondrocyte by HES1 overexpression

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