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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Makoto Ikeya

PROVIDER: E-GEOD-62783 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Neofunction of ACVR1 in fibrodysplasia ossificans progressiva.

Hino Kyosuke K Ikeya Makoto M Horigome Kazuhiko K Matsumoto Yoshihisa Y Ebise Hayao H Nishio Megumi M Sekiguchi Kazuya K Shibata Mitsuaki M Nagata Sanae S Matsuda Shuichi S Toguchida Junya J

Proceedings of the National Academy of Sciences of the United States of America 20151130 50

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease characterized by extraskeletal bone formation through endochondral ossification. FOP patients harbor point mutations in ACVR1 (also known as ALK2), a type I receptor for bone morphogenetic protein (BMP). Two mechanisms of mutated ACVR1 (FOP-ACVR1) have been proposed: ligand-independent constitutive activity and ligand-dependent hyperactivity in BMP signaling. Here, by using FOP patient-derived induced pluripotent stem cells (F ...[more]

PMID: 26621707

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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

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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.

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2010-07-30 | E-GEOD-22637 | biostudies-arrayexpress

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