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Optic Nerve Head Spatial Transcriptomic Change in Non-Human Primate Early Experimental Glaucoma.

ABSTRACT: Purpose: To determine optic nerve head (ONH) laminar collagen and retrolaminar myelin expression change in non-human-primate (NHP) experimental-glaucoma (EG) using immunohistochemistry (IHC) and spatial transcriptomics. Methods: Unilateral EG NHPs (n=3) were perfusion fixed, ONHs were trephined, embedded in paraffin and serial sectioned for IHC and spatial transcriptomics. EG versus control eye retinal nerve fiber layer thickness (RNFLT) and axon loss within each region of study were estimated. Results: CNPase levels decrease in the retrolaminar region of the ONH in early EG by IHC. Multiple myelin genes are decreased in early NHP EG in the retrolaminar region. Inflammatory pathways were upregulated in the retrolaminar region as well. Among the top genes that were altered in the laminar region were collagen related genes and Transforming Growth Factor Beta 1 (TGFβ1). Conclusions: Spatial transcriptomics analysis revealed a consistent downregulation of multiple myelin-related genes, while IHC confirmed a corresponding decrease in CNPase protein expression. Importantly, spatial transcriptomics identified differential profiles among the prelaminar, laminar, and retrolaminar ONH. Together, these findings highlight early myelin disruption and provide insights into the spatial and molecular dynamics of disease onset in NHP. This work advances our understanding of glaucoma pathogenesis and lays the groundwork for developing novel therapeutic strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE316553 | GEO | 2026/03/18

REPOSITORIES: GEO

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Project description:The majority of transplanted organs are recovered from deceased donors after brain death (BD). BD has been hypothesized to compromise organ quality in part from the activation of systemic inflammation. The objective of this study was to characterize the immune response induced by BD in a well controlled non-human primate (NHP) model. Assessment of physiologic parameters (blood pressure, heart rate, urinary output, catecholamines, and cerebral angiograms) was used to confirm BD. After 6h of BD, we monitored changes in the peripheral blood by flow cytometry, liver gene expression by microarray and liver protein expression by Western blotting and immunohistochemistry (IHC). BD was indicated by a rapid increase in blood pressure followed by hemodynamic instability, hypotension, diabetes insipidus and the absence of cerebral blood flow and brain stem reflexes. Within the peripheral blood IL-6 levels and neutrophils increased and myeloid dendritic cells decreased in BD NHP when compared to living donor controls. Genes related to innate inflammatory response and apoptosis were significantly upregulated in BD NHP. BD livers showed increased expression of suppressor of cytokine signaling 3 (SOCS3) protein and the danger associated molecular pattern protein S100A9. Increased expression of intracellular cellular adhesion molecule 1 (ICAM-1) and major histocompatibility complex (MHC) II, neutrophil accumulation, and products of oxidative stress (carboxy methyl lysine (CML) and hydroxynonenal (HNE)) were detected by IHC in livers. Conclusion: These data indicate that BD leads to the rapid activation of an inflammatory response within the liver involving components of the innate immune response at the gene and protein levels. The activation of these inflammatory pathways may provide one explanation for the reduced post-transplant function of organs from brain dead donors. Microarray analysis was performed to compare gene expression patterns from livers recovered after 5 hours of brain death (n=5) and from "living donor" non-brain dead controls (n=5).

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Optic Nerve Head Spatial Transcriptomic Change in Non-Human Primate Early Experimental Glaucoma.

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