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Key Regulatory Networks of Mitochondrial Dysfunction in Human Hippocampal Neurons under Cobaltous Chloride-Induced Hypoxia Revealed by Combined Transcriptome Analysis with Protein-Protein Interaction

ABSTRACT: Hypoxic stress in hippocampal neurons is a key factor in the pathogenesis of neurodegenerative diseases, yet the underlying gene regulatory networks remain unclear. Here, we exposed human hippocampal neuronal cells (HPPNCs) to CoCl₂-induced hypoxia and performed transcriptome sequencing alongside morphological and functional assays. We identified substantial mitochondrial damage and significant depolarization of mitochondrial membrane potential under hypoxic conditions. RNA-seq analysis revealed 471 differentially expressed genes (DEGs) enriched in pathways related to oxygen sensing, metabolic reprogramming, angiogenesis, and synaptic function. Protein-protein interaction analysis, molecular docking, and ceRNA network construction highlighted HSPD1, HSPA9, and HSP90AA1 as central regulators of mitochondrial quality control and adaptation to hypoxic stress. For transcriptome analysis, total RNA was extracted, polyA-selected, and strand-specific libraries with ~400 bp inserts were prepared. Paired-end 150 bp sequencing was performed on an Illumina NovaSeq X Plus platform with three biological replicates per group. The dataset includes raw sequencing files and processed gene expression matrices, which are publicly available in this GEO submission.

ORGANISM(S): Homo sapiens

PROVIDER: GSE345556 | GEO | 2026/09/05

REPOSITORIES: GEO

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Project description:Background: Hypoxic injury is a critical pathological factor in various retinal degenerative diseases, leading to mitochondrial dysfunction and irreversible loss of retinal neurons. This study investigated the neuroprotective potential of Icariin-loaded extracellular vesicles (EV_ICA) using both R28 retinal progenitor cells and human embryonic stem cell (hESC)-derived retinal organoids. Methods: EV_ICA were isolated and characterized by morphology, EV marker expression, and zeta potential analysis. A CoCl₂-induced hypoxic injury model was established in R28 cells and hESC-derived retinal organoids to evaluate the therapeutic effects of EV_ICA. Gene and protein expression analyses, bulk RNA sequencing (RNA-seq), gene set enrichment analysis (GSEA), mitochondrial ROS measurements, and intracellular ATP assays were performed to assess neuroprotective efficacy and mitochondrial function. Results: EV_ICA exhibited typical spherical morphology, expressed standard EV markers, and showed a shift toward a less negative zeta potential compared to Naïve EV. In hypoxia-injured retinal models, EV_ICA significantly restored the expression of key retinal and neuroprotective markers, including Syntaxin12, NeuN, Vegf, Rbpms, Brn-3a, and Bdnf, while suppressing Hif-1α accumulation. Transcriptomic and GSEA analyses revealed that EV_ICA reactivated biological pathways associated with phototransduction, visual perception, and retinal development that were impaired under hypoxic conditions. Furthermore, EV_ICA improved mitochondrial homeostasis by up-regulating mitochondrial-related genes, reducing mitochondrial ROS accumulation, and recovering intracellular ATP production. Conclusion: These findings demonstrate that EV_ICA exerts neuroprotective effects by preserving mitochondrial quality control and restoring functional retinal gene programs under hypoxic stress. EV_ICA may therefore serve as a promising therapeutic candidate for hypoxia-related retinal degeneration and provide potential applications for cell-free regenerative medicine

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Key Regulatory Networks of Mitochondrial Dysfunction in Human Hippocampal Neurons under Cobaltous Chloride-Induced Hypoxia Revealed by Combined Transcriptome Analysis with Protein-Protein Interaction

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