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Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD

ABSTRACT: Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD

PROVIDER: PRJNA949182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23979309.fastq.gz	Fastqsanger.gz
	SRR23979310_1.fastq.gz	Fastqsanger.gz
	SRR23979310_2.fastq.gz	Fastqsanger.gz
	SRR23979311_1.fastq.gz	Fastqsanger.gz
	SRR23979311_2.fastq.gz	Fastqsanger.gz

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Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scRNA-seq]

Project description:Wet age-related macular degeneration (AMD), characterized by leaky neovessels emanating from the choroid, is a main cause of blindness. As current treatments for wet AMD require regular intravitreal injections of anti-VEGF biologics, there is a need for the novel development of less invasive treatments. Here, we developed a novel inhibitor of microtubule-associated End Binding 3 protein (EB3), herein termed EBIN, which blocked pathological Ca2+ signaling in activated endothelial cells and suppressed leakage of choroidal neovessels. Delivery of EBIN via eye drops in mouse and non-human primate (NHP) models of AMD prevented neovascular leakage and neovascularization as effectively as intravitreal injection of anti-VEGF therapy. EBIN activated Meis2-Pax6 regenerative pathways in metabolic-active endothelial cells comprising neovessels and promoted tissue regeneration. Furthermore, single nuclei assay for transposase-accessible chromatin sequencing (sn-ATAC-seq) analysis demonstrated that in metabolic-active endothelial cells, the RPE, and photoreceptors, EBIN induced global increases in chromatin accessibility, the biological process progressively inhibited in AMD patients. These results suggest the unique therapeutic mode of action of this novel drug candidate, which can potentially promote regeneration of eye tissue by reversing the degenerative processes underlying both the neovascular and atrophic forms of AMD.

2023-08-30 | GSE228273 | GEO

Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scATAC-seq]

2023-08-30 | GSE228270 | GEO

Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [RNA-seq]

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Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scATAC-seq]

Project description:Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scATAC-seq]

| PRJNA949176 | ENA

Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [RNA-seq]

Project description:Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [RNA-seq]

| PRJNA949174 | ENA

Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scRNA-seq]

Project description:Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD [scRNA-seq]

| PRJNA949184 | ENA

Inhibition of EB3 activates the Meis2-Pax6 regenerative program in wet AMD

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-30 | GSE228276 | GEO

Single-cell transcriptome of wet AMD patient-derived endothelial cells in angiogenic sprouting

Project description:Age-related macular degeneration (AMD) is a global leading cause of visual impairment in older populations. ‘Wet’ AMD, the most common subtype of this disease, occurs when pathological angiogenesis infiltrates the subretinal space (choroidal neovascularization), causing hemorrhage and retinal damage. Gold standard anti-vascular endothelial growth factor (VEGF) treatment is an effective therapy, but the long-term prevention of visual decline has not been as successful. This warrants the need to elucidate potential VEGF-independent pathways. We generated blood out-growth endothelial cells (BOECs) from wet AMD and normal control subjects, then induced angiogenic sprouting of BOECs using a fibrin gel bead assay. To deconvolute endothelial heterogeneity, we performed single-cell transcriptomic analysis on the sprouting BOECs, revealing a spectrum of cell states. Our wet AMD BOECs share common pathways with choroidal neovascularization such as extracellular matrix remodeling that promoted proangiogenic phenotype, and our ‘activated’ BOEC subpopulation demonstrated proinflammatory hallmarks, resembling the tip-like cells in vivo. We uncovered new molecular insights that pathological angiogenesis in wet AMD BOECs could also be driven by interleukin signaling and amino acid metabolism. A web-based visualization of the sprouting BOEC single-cell transcriptome (https://christinecheunglab.shinyapps.io/human_wet_AMD_sprouting/) has been created to facilitate further discovery research.

2022-11-02 | GSE213933 | GEO

Single-cell transcriptome of wet AMD patient-derived endothelial cells in angiogenic sprouting

Project description:Single-cell transcriptome of wet AMD patient-derived endothelial cells in angiogenic sprouting

| PRJNA883213 | ENA

Stability of the neuronal fate determinant MEIS2 is controlled by calpain2

Project description:Calpains are non-lysosomal, Ca2+-dependent cysteine proteases, which are associated with various cellular functions but have so far been mainly studied in the context of disease. Their contribution to homeostasis in the healthy organism is still not well understood and their substrates have remained enigmatic in most cases. In the present study, we describe a previously unrecognized role for the calpain protease calpain2 in the regulation of neuronal differentiation of adult neural stem- and progenitor cells through cleavage and elimintation of the neuronal fate determinant MEIS2. Mass spectrometry analysis was performed on immunoprecipitated MEIS2 protein to identify phosphory¬lated residues in MEIS2 and on immunoprecipitated MEIS2 incubated with native porcine calpain2 to map calpain2-induced cleavage sites in the protein.

2024-02-08 | PXD036442 | Pride

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