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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal low-dose Propofol exposure

ABSTRACT: The regulation of gene expression after low-dose Propofol exposured in neural stem / progenitor cells (NSPCs)

ORGANISM(S): Mus musculus

PROVIDER: GSE200968 | GEO | 2022/08/17

REPOSITORIES: GEO

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal subclinical dose of Propofol exposure revealed by single-nuclei transcriptomic profiling

Project description:The change of cell lineage and regulation of gene expression after low-dose Propofol exposured in hippocampal of PND10 mice

2022-08-17 | GSE186216 | GEO

Effects of Propofol Treatment in Neural Progenitors Derived from Human Induced Pluripotent Stem Cells

Project description:Propofol is an intravenous anesthetic that has been widely used in the clinical setting. Besides its anesthetic effects, propofol has been reported to influence the regulation of autonomic system. Controversies exist with regards to whether propofol exposure is safe for pregnant women and young children. The recent emergence of human induced pluripotent stem cells (hiPSCs) has provided a promising and theoretically inexhaustible source of neural progenitor cells (NPCs) for drug testing, which could be extended to in vitro experiments for anesthetics such as propofol. NPCs derived from three hiPSC lines, NES-GFP (a NESTIN-GFP reporter), USCK7 (iPSCs derived from urine derived cells), and ND2-0 (NIH), were treated with propofol at different concentrations (20, 50, 100 and 300 µM) for 6 h or 24 h. Early and late cell injury, cell proliferation and apoptosis were evaluated. Comparison of genome-wide gene expression profiles was performed for propofol-treated and untreated control iPSC-NPCs. Propofol treatment of NPCs for 6 h at the clinically relevant concentration (20 or 50 µM) did not affect cell viability, apoptosis, or proliferation, while propofol at higher concentration (100 or 300 µM) decreased NPC viability and induced apoptosis. Prolonged treatment of propofol for 24 h significantly decreased cell viability. In addition, 20 µM propofol treatment for 6 h did not alter global gene expression. Higher concentration of propofol exerted potential cytotoxicity via multiple cellular mechanisms. In summary, propofol treatment at commonly practiced clinical doses for 6 h did not have adverse effects on hiPSC-derived NPCs. In contrast, longer exposure and/or higher concentration of propofol treatment could decrease NPC viability and induce apoptosis.

2017-07-21 | GSE101724 | GEO

Disturbance of key cellular subproteomes upon propofol treatment is associated with increased permeability of the blood-brain barrier

Project description:Background: Propofol is a short-acting anesthetic, which is often used for induction and maintenance of general anesthesia, sedation for mechanically ventilated adults and procedural sedation. Several side effects of propofol are known and a substantial number of patients suffer from post-operative delirium after propofol application. In this study, we analyzed the effect of propofol on the function and protein expression profile on a proteome-wide scale. Methods: We cultured human brain microvascular endothelial cells in the absence and presence of propofol and analyzed the permeability of the blood-brain barrier (BBB) by fluorescein passage and protein expression on a proteome-wide scale by mass spectrometry. Results: Propofol interfered with the function of the blood-brain barrier. This was not due to de-creased adhesion of propofol-treated human brain microvascular endothelial cells. The proteomic analysis revealed that some key pathways in these cells were disturbed, such as oxygen metabolism, DNA damage recognition and response to stress. Conclusions: Propofol has strong effects on protein expression which could explain several side effects of propofol.

2022-10-13 | PXD033856 | Pride

Propofol alters the mRNA profile in the developing mouse hippocampus

Project description:Propofol has been found to be toxic to developing neurons. The goal of the current study was to nominate novel genes predicted to underly the neurotoxicity, and use these candidates for future functional pathway assessment

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Gene expression of brain regions activated by sevoflurane and propofol

Project description:The basic mechanisms of action for general anesthesia are not fully understood. We thought differences in the neural activation sites of different types of anesthetics and differences in gene expression changes in those brain regions may lead to differences in the incidence of side effects. We performed gene expression analysis using microarrays in the identified regions that have been related to the mechanisms of anesthetic action and side effects. Gene expression changes in these brain regions were determined for sevoflurane and propofol to understand the mechanisms that cause differences among anesthetics.

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Expression data from proliferating and quiescent adult hippocampal neural stem and progenitor cells

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