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

ABSTRACT: Comparison of gene expressions among FOP- or resFOP-iMSCs after chondrogenic differentiation with Activin-A, BMP-7 or TGF-B3

ORGANISM(S): Homo sapiens

PROVIDER: GSE90638 | GEO | 2017/12/01

SECONDARY ACCESSION(S): PRJNA355267

REPOSITORIES: GEO

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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.

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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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Homo sapiens

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

| PRJNA355267 | ENA