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FOP HO early lesion single cell sequencing

ABSTRACT: experiment for single cell sequencing of early FOP lesion to determine the pathogenesis of HO lesion development

ORGANISM(S): Mus musculus

PROVIDER: GSE304287 | GEO | 2025/08/08

REPOSITORIES: GEO

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FOP HO early lesion single cell sequencing

Project description:FOP HO early lesion single cell sequencing

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Recapitulation of the pro-inflammatory signature of monocytes with ACVR1 mutation using FOP patient-derived iPSCs

Project description:Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease characterized by progressive heterotopic ossification (HO) in soft tissues due to a heterozygous mutation of the ACVR1A/ALK2 gene (FOP-ACVR1A), which erroneously transduces the BMP signal by Activin-A. Although inflammation is known to trigger HO in FOP, the role of FOP-ACVR1A on inflammatory cells remains to be elucidated. Here we investigated this issue using immortalized monocytic cell lines from FOP-iPSCs (FOP-ML) and mutation-rescued iPSCs (resFOP-ML). Without any stimulation, FOP-ML showed the pro-inflammatory signature of CD16+ monocytes with an up-regulation of INHBA gene, and treatment of resFOP-ML with Activin-A induced an expression profile consistent with FOP-ML at baseline. Treatment of FOP-ML with Activin-A further induced the inflammatory profile with the up-regulation of inflammation-associated genes, some of which were suppressed by corticosteroid. Experiments using an inhibitor for TGFβ or BMP signals demonstrated that Activin-A-induced genes, such as CD16 and CCL7, were regulated by both signals, indicating Activin-A transduced dual signals in FOP-ML. A comparison with resFOP-ML identified several down-regulated genes in FOP-ML, including LYVE-1, which is known to suppress matrix-formation in vivo. The down-regulation of LYVE-1 in HO tissues was confirmed in FOP model mice, verifying the in vitro experiments. These results indicate that FOP-ML faithfully recapitulated the phenotype of primary monocytes in FOP and its combination with resFOP-ML is useful for investigating the molecular events at the initial inflammation stage of HO in FOP.

2022-05-12 | GSE183525 | GEO

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Project description:We described a genetic map of PBMCs in FOP patients by using single-cell RNA sequencing for the first time.

2024-07-01 | GSE156464 | GEO

Control and FOP Human iPSC derived myogenic cell single cell RNA sequencing

Project description:We compared the transcriptome of sorted muscle stem/progenitor cells differentiated from control and FOP (ACVR1 R206H (c.617>A)) human induced pluripotent stem cells.

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Global gene expression profiling of FOP- or resFOP-iMSCs after chondrogenic differentiation

Project description:Comparison of gene expressions among FOP- or resFOP-iMSCs after chondrogenic differentiation with or without Activin-A. Comparison of gene expressions among FOP- or resFOP-iMSCs after chondrogenic differentiation with or without Activin-A.

2015-12-09 | E-GEOD-69459 | biostudies-arrayexpress

Global gene expression profiling of FOP- or resFOP-iMSCs treated by several ligands

Project description:Analyzed differentially expressed genes among FOP- or resFOP-iMSCs treated by several ligands: Activin-A, 100 ng/mL; BMP-7, 100 ng/mL; TGF-B3, 10 ng/mL Comparison of gene expressions among FOP- or resFOP-iMSCs treated 16h by several ligands

2015-12-09 | E-GEOD-62783 | biostudies-arrayexpress

RNA data of human FOP patients-derived iPSCs treated with ACVR1 R206H mutant-targeting AAVs

Project description:We found that both A9 (amiR-RH6) and A10 (amiR-RH7)-AAVs significantly decrease osteogenic differentiation of FOP-iPSCs. We also observed that A9 and A10-AAVs treatment changed the ratio of R206H mutant to wildtype of ACVR1 in FOP-iPSCs. To identify off-target effect of A9 or A10-AAVs, we compared RNA expression of FOP-iPSCs treated with control, A9, or A10-AAVs.

2022-09-20 | GSE213579 | GEO

Hydrogenobaculum sp. HO strain:HO

Project description:Hydrogenobaculum sp. HO genome sequencing project

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Transcriptome data of Alcaligenes sp. HO-1 in response to ammonium stimulation at several time points.

Project description:A heterotrophic ammonia-oxidizing bacterium Alcaligenes sp. HO-1 was isolated from the activated sludge of a bioreactor treating ammonia-rich piggery wastewater. The goal and objectives of this experiment are to analyze the transcriptome profiles of nitrogen-metabolism-related genes of Alcaligenes sp. HO-1 in response to ammonium stimulation over time and to find out potential genes involved in ammonia oxidation process. So the RNA-seq anaylsis was performed by setting up each time points (0, 3.5, 10, 22 hours) when strain HO-1 were exposed to ammonia. HO-1 was cultured with 83 mM succinate and 14 mM ammonium sulfate until ammonia was completely consumed and then another 14 mM of ammonium sulfate was added to the culture. Cells were harvested at 0 h, 3.5 h, 10 h and 22 h after the addition of ammonium sulfate. The sequencing data of RNAs obtained from strain HO-1 cells at each time was analyzed.

2022-05-20 | GSE174685 | GEO

Gene expression signatures of HO-1 in BeWo cells

Project description:Heme Oxygenase-1 (HO-1) is expressed in many cancers and influences the growth, survivall and metastasis of tumors, however, the molecular mechanisms remains largely unknown. To identify a common mechanism of action of HO-1 in cancer, we studied the global effect of HO-1 on the transcriptome of multiple tumors. Genome-wide expression profiling of HO-1 expressing versus HO-1 silenced cancer cells and a further data mining analysis of the preexisting expression database of 190 human tumors of 14 cancer types led us to identify 14 genes, the expression of which correlated firmly and universally with that of HO-1 (P < 0.001). These genes included regulators of cell plasticity and extracellular matrix remodeling (MMP2, ADAM8, TGFβ1, BGN, COL21A1, PXDN), signaling (CRIP2, MICB), amino acid transport and glycosylation (SLC7A1 and ST3GAL2), estrogen and phospholipid biosynthesis (AGPAT2 and HSD17B1), protein stabilization (IFI30) and phosphorylation (ALPPL2). PXDN, one of the genes being co-expressed with HO-1, was selected for further analysis. Immunofluorescence and western blotting confirmed positive correlation of PXDN with HO-1 levels in BeWo cancer cells as well as co-localization in invasive extravillous trophoblast cells of first trimester placenta. Loss of HO-1 in BeWo cells correlated with reduced cell adhesion to Collagen type I, Fibronectin and Laminin. The adhesion-promoting effects of HO-1 were dependent on PXDN expression, as loss of PXDN in HO-1 expressing BeWo cells led to reduced cell attachment to Laminin and Fibronectin coated wells.

2011-02-15 | GSE20404 | GEO

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