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SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.

ABSTRACT: SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.

PROVIDER: PRJNA721686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14230872_1.fastq.gz	Fastqsanger.gz
	SRR14230872_2.fastq.gz	Fastqsanger.gz
	SRR14230873_1.fastq.gz	Fastqsanger.gz
	SRR14230873_2.fastq.gz	Fastqsanger.gz
	SRR14230874_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.

Project description:Osteoclasts are multinucleated bone resorbing cells, and their dysregulation leads to pathological bone destruction. Osteoclast formation must be tightly regulated to prevent excessive bone loss and to minimize bone damage. SREBP2 is a key transcription factor for cholesterol biosynthesis and a sensor for intracellular lipids. However, how the crosstalk between SREBP2 and lipid metabolism contributes to osteoclasts has not been determined. Here, we reveal that SREBP2 is a negative regulator of osteoclastogenesis. Targeted deletion of SREBP2 in myeloid cells result in low bone mass and accelerates inflammatory bone destruction. SREBP2-mediated regulation of osteoclastogenesis is independent of its canonical function in cholesterol biosynthesis but is mediated, in part, by its downstream target, interferon regulatory factor (IRF)7. Taken together, our study highlights the SREBP2-IRF7 regulatory circuit forms as a negative feedback inhibitory loop in osteoclast differentiation that represents a novel mechanism to restrain deleterious pathological bone destruction.

2024-09-30 | GSE172007 | GEO

SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.

Project description:Osteoclasts are multinucleated bone-resorbing cells, and their formation is tightly regulated to prevent excessive bone loss. However, the mechanisms by which osteoclast formation is restricted remain incompletely determined. Here, we found that sterol regulatory element binding protein 2 (SREBP2) functions as a negative regulator of osteoclast formation and inflammatory bone loss. Cholesterols and SREBP2, a key transcription factor for cholesterol biosynthesis, increased in the late phase of osteoclastogenesis. The ablation of SREBP2 in myeloid cells resulted in increased in vivo and in vitro osteoclastogenesis, leading to low bone mass. Moreover, deletion of SREBP2 accelerated inflammatory bone destruction in murine inflammatory osteolysis and arthritis models. SREBP2-mediated regulation of osteoclastogenesis is independent of its canonical function in cholesterol biosynthesis but is mediated, in part, by its downstream target, interferon regulatory factor 7 (IRF7). Taken together, our study highlights a previously undescribed role of the SREBP2-IRF7 regulatory circuit as a negative feedback loop in osteoclast differentiation and represents a novel mechanism to restrain pathological bone destruction.

| S-EPMC11350122 | biostudies-literature

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses

Project description:This SuperSeries is composed of the following subset Series: GSE36241: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq) GSE37051: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression) Refer to individual Series

2012-09-19 | E-GEOD-37052 | biostudies-arrayexpress

Acod1-mediated effect on osteoclast differentiation

Project description:Enhanced osteoclast-mediated bone erosion is a prominent hallmark of rheumatoid arthritis. Emerging evidence suggests that this process is facilitated by metabolic dysregulation of osteoclasts. The mitochondrial enzyme aconitate decarboxylase 1 (Acod1, also known as immune responsive gene 1 [Irg1]) serves as a mediator between the metabolic condition and the functional state of different types of cells. Acod1-deficient mice are characterized by enhanced osteoclast differentiation and bone erosion in an inflammatory arthritis model, while therapeutic treatment with the itaconate-derivative 4-octyl-itaconate (4-OI) alleviates the disease phenotype in experimental arthritis. To ascertain the influence of the Acod1-itaconate axis on the genomic transcriptional network of osteoclasts, we performed a whole transcriptome RNA sequencing analysis with fully differentiated osteoclasts from WT and Acod1-deficient mice that were cultured in the presence or absence of 4-OI.

2024-07-15 | GSE237504 | GEO

Investigation of Genomic RNA Polymerase II-Rich Locations in Osteoclast Precursor Cells

2022-11-01 | GSE203355 | GEO

RNA Sequencing Analysis of Osteoclast Precursor Cells under Dexamethasone Stimulation

Project description:Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a refractory joint disease caused by prolonged and excessive use of glucocorticoids (GCs). Excessive osteoclast activation has been implicated in the pathological bone erosion of GIONFH. Our previous study found that dexamethasone (10-8M) stimulation significantly enhances osteoclast formation in vitro. To identify therapeutic targets for GIONFH by characterizing glucocorticoid-driven transcriptional alterations in osteoclastogenesis, we performed RNA sequencing on osteoclast precursor cells (OPCs) under RANKL (25ng/ml) and Dex condition (treated with RANKL (25ng/ml) and Dex(10-8M) ) for 24 hours.

2025-05-30 | GSE298117 | GEO

Strand-Specific Nuclear Transcriptome Analysis of Osteoclast Precursor Cells

Project description:To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. In this dataset, we validated the presence of the predicted SE-eRNAs.

2022-11-01 | GSE203359 | GEO

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq)

Project description:We predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway. C57BL/6 mice were obtained from Jackson Laboratories. Foxo3-/- mice in the FVB background were obtained from MMRRC and were backcrossed to C57BL/6 mice at least 5 times to generate congenic mice. C57BL/6 Foxo3+/- heterozygotes were intercrossed to generate Foxo3-/- mice. Mice were maintained at the animal facility of the Institute for Systems Biology and used at 8–12 weeks of age. All animals were housed and handled according to the approved protocols of University of Washington and Institute for Systems Biology's Institutional Animal Care and Use Committees.

2012-09-19 | E-GEOD-36241 | biostudies-arrayexpress

Effects of Intestine-specifc SREBP2 overactivation on gene expression in mouse jejnum

Project description:The active form of the SREBP2 transcription factor was specifically overexpressed in the intesitne. This was achieved by generating transgenic mouse model (designated as ISR2) in which the transgene represents the N-terminal active SREBP2 transcription factor driven by the villin promoter. In this project, we investigated the effects of overactivation of SREBP2 on gene expression in mouse jejunum Gene expression profile in the jejunum of ISR2 was compared to gene expression profile in the jejunum of their wild type littermates.

2013-10-26 | E-GEOD-51736 | biostudies-arrayexpress

Base-Level Resolution Run-On Sequencing in Osteoclast Precursor Cells

Project description:To understand the pathogenic mechanisms of bone erosion in rheumatoid arthritis (RA), we investigated osteoclast-specific epigenetic programs, RANKL-responsive super-enhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) in human osteoclasts. This dataset contains precision run-on sequencing (PRO-seq) data performed to detect SE-eRNA transcription activity.

2022-11-01 | GSE203356 | GEO

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