Similar Datasets
Project description:Epilepsy is a neurological disorder characterised by recurrent spontaneous seizures. Approximately 30% of patients are unable to achieve adequate seizure control with available medications, highlighting the need to better understand disease mechanisms and develop improved treatments. Mesial temporal lobe epilepsy (MTLE) is a common subtype of treatment-resistant epilepsy. Patients with MTLE often have experienced a prior neurological insult, such as a traumatic brain injury, or status epilepticus (SE), that is believed to contribute to epileptogenic changes that lead to MTLE. However, the molecular mechanisms underlying epileptogenesis remain incompletely understood. Extracellular vesicles (EVs) are small membrane-bound particles released by cells that are important for intercellular communication. Recent studies identified altered microRNA (miRNA) content in brain-derived EVs (BDEVs) in models of MTLE, but whether BDEV function is altered has not been explored. Using the pilocarpine mouse model of MTLE, we examined the effects of SE on the function and miRNA cargo of hippocampal BDEVs during the epileptogenic period. BDEVs were isolated from hippocampi of control and pilocarpine-treated mice 24 h after SE. To assess functional changes, we compared gene expression in N2a neuronal-like cells and BV2 microglial-like cells exposed to control BDEVs (CON-BDEVs) or BDEVs collected after SE (SE-BDEVs). SE-BDEVs induced distinct transcriptional changes in N2a cells including alterations in the expression of genes related to TGF-β signalling, amino acid regulation of mTORC1 and neurotransmitter signalling. In BV2 cells, SE-BDEVs increased the expression of genes associated with inflammatory cytokine release. Analysis of BDEV miRNA content revealed multiple differentially expressed miRNAs between SE- and CON-BDEVs, with predicted targets overlapping with genes uniquely altered by SE-BDEVs. Notably, SE-induced miRNA changes were still observed 10 days post-SE, indicating sustained modulation of BDEV cargo. These findings identify SE-induced alterations in both the function and miRNA composition of hippocampal BDEVs, suggesting that BDEVs may contribute to epileptogenesis in MTLE.
2026-06-18 | GSE327584 | GEO
Project description:Epilepsy is a neurological disorder characterised by recurrent spontaneous seizures. Approximately 30% of patients are unable to achieve adequate seizure control with available medications, highlighting the need to better understand disease mechanisms and develop improved treatments. Mesial temporal lobe epilepsy (MTLE) is a common subtype of treatment-resistant epilepsy. Patients with MTLE often have experienced a prior neurological insult, such as a traumatic brain injury, or status epilepticus (SE), that is believed to contribute to epileptogenic changes that lead to MTLE. However, the molecular mechanisms underlying epileptogenesis remain incompletely understood. Extracellular vesicles (EVs) are small membrane-bound particles released by cells that are important for intercellular communication. Recent studies identified altered microRNA (miRNA) content in brain-derived EVs (BDEVs) in models of MTLE, but whether BDEV function is altered has not been explored. Using the pilocarpine mouse model of MTLE, we examined the effects of SE on the function and miRNA cargo of hippocampal BDEVs during the epileptogenic period. BDEVs were isolated from hippocampi of control and pilocarpine-treated mice 24 h after SE. To assess functional changes, we compared gene expression in N2a neuronal-like cells and BV2 microglial-like cells exposed to control BDEVs (CON-BDEVs) or BDEVs collected after SE (SE-BDEVs). SE-BDEVs induced distinct transcriptional changes in N2a cells including alterations in the expression of genes related to TGF-β signalling, amino acid regulation of mTORC1 and neurotransmitter signalling. In BV2 cells, SE-BDEVs increased the expression of genes associated with inflammatory cytokine release. Analysis of BDEV miRNA content revealed multiple differentially expressed miRNAs between SE- and CON-BDEVs, with predicted targets overlapping with genes uniquely altered by SE-BDEVs. Notably, SE-induced miRNA changes were still observed 10 days post-SE, indicating sustained modulation of BDEV cargo. These findings identify SE-induced alterations in both the function and miRNA composition of hippocampal BDEVs, suggesting that BDEVs may contribute to epileptogenesis in MTLE.
2026-06-18 | GSE327583 | GEO
Project description:Epilepsy is a neurological disorder characterised by recurrent spontaneous seizures. Approximately 30% of patients are unable to achieve adequate seizure control with available medications, highlighting the need to better understand disease mechanisms and develop improved treatments. Mesial temporal lobe epilepsy (MTLE) is a common subtype of treatment-resistant epilepsy. Patients with MTLE often have experienced a prior neurological insult, such as a traumatic brain injury, or status epilepticus (SE), that is believed to contribute to epileptogenic changes that lead to MTLE. However, the molecular mechanisms underlying epileptogenesis remain incompletely understood. Extracellular vesicles (EVs) are small membrane-bound particles released by cells that are important for intercellular communication. Recent studies identified altered microRNA (miRNA) content in brain-derived EVs (BDEVs) in models of MTLE, but whether BDEV function is altered has not been explored. Using the pilocarpine mouse model of MTLE, we examined the effects of SE on the function and miRNA cargo of hippocampal BDEVs during the epileptogenic period. BDEVs were isolated from hippocampi of control and pilocarpine-treated mice 24 h after SE. To assess functional changes, we compared gene expression in N2a neuronal-like cells and BV2 microglial-like cells exposed to control BDEVs (CON-BDEVs) or BDEVs collected after SE (SE-BDEVs). SE-BDEVs induced distinct transcriptional changes in N2a cells including alterations in the expression of genes related to TGF-β signalling, amino acid regulation of mTORC1 and neurotransmitter signalling. In BV2 cells, SE-BDEVs increased the expression of genes associated with inflammatory cytokine release. Analysis of BDEV miRNA content revealed multiple differentially expressed miRNAs between SE- and CON-BDEVs, with predicted targets overlapping with genes uniquely altered by SE-BDEVs. Notably, SE-induced miRNA changes were still observed 10 days post-SE, indicating sustained modulation of BDEV cargo. These findings identify SE-induced alterations in both the function and miRNA composition of hippocampal BDEVs, suggesting that BDEVs may contribute to epileptogenesis in MTLE.
2026-06-18 | GSE327585 | GEO
Project description:Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [BV2-RNA-seq]
| PRJNA1451481 | ENA
Project description:Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [miRNA_10Day]
| PRJNA1451477 | ENA
Project description:Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [miRNA-24hr]
| PRJNA1451478 | ENA
Project description:Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [N2A-RNA-Seq]
| PRJNA1451476 | ENA
Project description:RiboTag mice B6N.129-Rpl22tm1.1Psam/J (# 011029, Jackson Laboratories), which carry a conditional Rpl22 allele (Sanz et al., 2009; doi: 10.1073/pnas.0907143106),were crossed with Pdgfb-iCreER mice that are tamoxifen-inducible form of Cre recombinase in vascular endothelial cells (Claxton et al., 2008; doi: 10.1002/dvg.20367),to generate Ribotag-Pdgf-β1 Cre mice
2023-09-20 | GSE223714 | GEO
Project description:Small extracellular vesicles (sEVs) were isolated from the culture supernatant of melanoma DCC-derived cell lines (MelDCC) after 48 hours of serum-free culture. sEVs were obtained through differential ultracentrifugation, specifically as the 100K pellet, following the protocol described in detail by Théry et al. (https://doi.org/10.1002/0471143030.cb0322s30). Proteomic analysis of the isolated sEVs was performed using mass spectrometry to characterize their protein content.
2025-02-24 | PXD059510 | Pride
Project description: Not available
| S-EPMC9546961 | biostudies-literature