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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

ABSTRACT: We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury and ripasudil treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE232746 | GEO | 2024/09/30

REPOSITORIES: GEO

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

2023-09-30 | GSE231358 | GEO

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

2023-09-30 | GSE233749 | GEO

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

2023-09-30 | GSE233750 | GEO

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

| PRJNA964468 | ENA

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

| PRJNA973685 | ENA

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

| PRJNA977695 | ENA

Smarcc1 drives optic stalk patterning and optic nerve head astrocyte differentiation

Project description:The optic nerve develops from the neuroectodermal optic stalk, which undergoes coordinated morphogenesis and gives rise to optic nerve astrocytes that support retinal ganglion cell (RGC) axons. Here, we define the progression of astrocyte formation from the optic stalk and identify stage‑specific functions of the SWI/SNF scaffolding subunits Smarcc1 (Baf155) and Smarcc2 (Baf170). Both factors are co‑expressed in retinal pigment epithelium (RPE) and optic stalk progenitors, with Smarcc2 persisting in differentiated RPE and astrocytes. Conditional deletion using Dct‑Cre revealed compensatory activity in pigmented lineages, whereas Smarcc1 loss uniquely disrupted optic nerve head (ONH) morphogenesis, resulting in glial lamina collapse, RGC degeneration, and progressive visual decline. Spatial transcriptomics and functional assays show that Smarcc1 enables dorsal optic stalk progenitors to transition from a pigmented, RPE‑like state to astrocyte progenitors by repressing pigment gene programs and permitting Pax2/Sox2 activity. After specification, Smarcc1 is also required for glial lamina assembly and astrocyte migration into the inner retina. These findings demonstrate that Smarcc1‑dependent chromatin remodeling coordinates astrocyte specification with ONH morphogenesis to maintain long‑term retinal function.

2026-06-29 | GSE336951 | GEO

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

| PRJNA977697 | ENA

Aldose reductase inhibition decelerates optic nerve degeneration by suppressing retinal microglia activation

Project description:To investigate the role of aldose reductase (AR) inhibition using Sorbinil on retinal microglia (RMG) activation, retinal ganglion cell (RGC) survival, and axon regeneration after optic nerve trauma. We observed that AR inhibition using Sorbinil attenuates RMG activation and subsequently promotes RGC survival and delays axon degeneration one week after optic nerve crush.

2023-04-05 | GSE200233 | GEO

Nuclear-localized HDAC4 promotes neuroprotection of retinal ganglion cells after optic nerve injury

Project description:Background: As the sole output neurons for the retina, retinal ganglion cells (RGCs) transmit all visual information from the retina via the optic nerve to the brain. RGCs do not regenerate when injured, and effective therapies for promoting RGC survival and axon regeneration in optic neuropathies comprise an unmet clinical need, including in the common disease glaucoma. Histone deacetylases (HDACs) are epigenetic modifiers that repress gene transcription and play a key role in retinal development and disease. In this study, we identify the role of HDAC4 in RGC neurodegeneration and axon regeneration. Methods: The role of HDAC4 in the regulation of RGC neuroprotection and axon regeneration was studied in the mouse optic nerve crush (ONC) model for optic neuropathy by transduction of RGCs in vivo with adeno-associated virus (AAV) vectors. HDAC4- and ONC-dependent gene expression in vivo were studied by single cell RNA sequencing (scRNA-seq) of isolated RGCs. Results: A loss-of-function screen for the role of HDACs in RGC survival after optic nerve crush (ONC) injury identified HDAC4 as essential element for RGC survival. Accordingly, expression of a constitutively nuclear HDAC4 S246/467/632A missense mutant (3SA) increased RGC survival and axon regeneration after ONC injury. Similar beneficial effects were conferred by expression of an N-terminal fragment of HDAC4 (HDAC4 NT) that constitutively represses gene expression. scRNA-seq showed that one day after ONC injury, transcriptomic profiles of RGCs were altered such that HDAC4 NT and to a lesser degree the HDAC4 3SA mutant attenuated the gene expression changes associated with injury. Conclusions: This study demonstrates that enhancement of nuclear HDAC4 activity will promote RGC survival and axon regeneration in the ONC model of RGC injury, identifying HDAC4 as a novel target in the development of therapeutics for RGC protection and restoration of visual function.

2026-01-01 | GSE252860 | GEO

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