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Exosomal miR-128-3p reversed fibrinogen-mediated inhibition of oligodendrocyte progenitor cell differentiation and remyelination after cerebral ischemia by targeting BMP signaling (miRNA-Seq)

ABSTRACT: To understand the mechanism by which fibrinogen inhibits OPC differentiation after ischemia and identify the precise target for reversing fibrinogen’s effects, OPCs were used for miRNA sequencing analysis. We then performed gene expression profiling analysis using data obtained from miRNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE206950 | GEO | 2022/12/31

REPOSITORIES: GEO

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Exosomal miR-128-3p reversed fibrinogen-mediated inhibition of oligodendrocyte progenitor cell differentiation and remyelination after cerebral ischemia by targeting BMP signaling

Project description:To understand the mechanism by which fibrinogen inhibits OPC differentiation after ischemia and identify the precise target for reversing fibrinogen’s effects, OPCs were used for mRNA sequencing analysis.

2022-12-31 | GSE206826 | GEO

Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_48h_Fibrinogen]

Project description:Determination of the mechanism by which fibrinogen, a central blood coagulation protein, regulates OPC functions and remyelination in the CNS. We used microarrays to determine the genes involved in OPC responses to fibrinogen, which is deposited in the CNS after blood-brain barrier disruption.

2017-11-02 | GSE104449 | GEO

Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_12h_Fibrinogen]

2017-11-02 | GSE104448 | GEO

BMP receptor blockade overcomes extrinsic inhibition of remyelination and restores neurovascular homeostasis

Project description:Extrinsic inhibitors at sites of blood-brain barrier (BBB) disruption and neurovascular damage contribute to remyelination failure in neurological diseases. However, therapies to overcome extrinsic inhibition of remyelination are not widely available and the dynamics of glial progenitor niche remodeling at site of neurovascular dysfunction are largely unknown. By integrating in vivo two-photon (2P) imaging co-registered with electron microscopy and transcriptomics in chronic neuroinflammatory lesions, we found repressed anticoagulation pathways in oligodendrocyte precursor cells (OPCs) that clustered perivascularly at sites of limited remyelination with deposition of fibrinogen, a blood coagulation factor abundantly deposited in multiple sclerosis lesions. By developing the OPC-X-screen to identify compounds that promote remyelination in the presence of extrinsic inhibitors, we showed that known promyelinating drugs did not rescue extrinsic inhibition of remyelination by fibrinogen. In contrast, bone morphogenetic protein (BMP) receptor blockade rescued the inhibitory fibrinogen effects and restored a promyelinating progenitor niche by promoting myelinating oligodendrocytes, while suppressing astrocyte cell fate with potent therapeutic effects in chronic models of multiple sclerosis. Thus, abortive OPC differentiation by fibrinogen is refractory to known promyelinating compounds, suggesting that blockade of the BMP signaling pathway may enhance remyelinating efficacy by overcoming extrinsic inhibition in neuroinflammatory lesions with vascular damage.

2021-08-24 | GSE166675 | GEO

Exosomal miR-128-3p reversed fibrinogen-mediated inhibition of oligodendrocyte progenitor cell differentiation and remyelination after cerebral ischemia.

Project description:AimsTo investigate the role of exosomal miR-128-3p in promoting fibrinogen-mediated inhibition of oligodendrocyte progenitor cell (OPC) differentiation and the therapeutic potential of exosomal miR-128-3p in cerebral ischemia.MethodsMouse models of middle cerebral artery occlusion (MCAO) were established as described previously. MCAO was treated with fibrinogen and exosomes by stereotactically injecting into the left stratum. Mouse cortical OPCs were used for mRNA and miRNA sequencing analysis. Exosomes were isolated from neural stem cells (NSCs) of mice.ResultsFibrinogen deposition suppressed remyelination after MCAO and inhibited OPC differentiation by activating ACVR1, the bone morphogenetic protein (BMP) signaling type I receptor. In vitro, miR-sequencing and verification studies revealed that miR-128-3p is associated with BMP signaling mediated by ACVR1. Additionally, transfer of NSC-derived exosomal miR-128-3p to OPCs significantly increased myelin basic protein expression and inhibited BMP signaling. Furthermore, NSC-derived exosomal miR-128-3p protected against fibrinogen-induced demyelination related to BMP signaling, reduced the infarct volume, and improved neurological function after MCAO.ConclusionsFibrinogen deposition inhibits remyelination after ischemic damage and NSC-derived exosomal miR-128-3p promotes OPC differentiation into OLs by suppressing BMP signaling, indicating that NSC-derived exosomal miR-128-3p represents a potential therapeutic target for ischemic stroke.

| S-EPMC10068474 | biostudies-literature

Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage

Project description:Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage

| PRJNA412647 | ENA

Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_12h_Fibrinogen]

Project description:Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_12h_Fibrinogen]

| PRJNA412657 | ENA

Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_48h_Fibrinogen]

Project description:Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_48h_Fibrinogen]

| PRJNA412656 | ENA

Exosomal miR-128-3p reversed fibrinogen-mediated inhibition of oligodendrocyte progenitor cell differentiation and remyelination after cerebral ischemia by targeting BMP signaling (miRNA-Seq)

Project description:Exosomal miR-128-3p reversed fibrinogen-mediated inhibition of oligodendrocyte progenitor cell differentiation and remyelination after cerebral ischemia by targeting BMP signaling (miRNA-Seq)

| PRJNA852950 | ENA

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage.

Project description:Blood-brain barrier (BBB) disruption alters the composition of the brain microenvironment by allowing blood proteins into the CNS. However, whether blood-derived molecules serve as extrinsic inhibitors of remyelination is unknown. Here we show that the coagulation factor fibrinogen activates the bone morphogenetic protein (BMP) signaling pathway in oligodendrocyte progenitor cells (OPCs) and suppresses remyelination. Fibrinogen induces phosphorylation of Smad 1/5/8 and inhibits OPC differentiation into myelinating oligodendrocytes (OLs) while promoting an astrocytic fate in vitro. Fibrinogen effects are rescued by BMP type I receptor inhibition using dorsomorphin homolog 1 (DMH1) or CRISPR/Cas9 activin A receptor type I (ACVR1) knockout in OPCs. Fibrinogen and the BMP target Id2 are increased in demyelinated multiple sclerosis (MS) lesions. Therapeutic depletion of fibrinogen decreases BMP signaling and enhances remyelination in vivo. Targeting fibrinogen may be an upstream therapeutic strategy to promote the regenerative potential of CNS progenitors in diseases with remyelination failure.

| S-EPMC5851281 | biostudies-literature

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