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Sevoflurane Induces a Cyclophilin D-Dependent Decrease of Neural Progenitor Cells Migration
Pan Lu1,2, Feng Liang2, Yuanlin Dong2
1Department of Anesthesia, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
Insights
Sevoflurane anesthesia impairs neural progenitor cell migration in young animals by increasing cyclophilin D (CypD) and reactive oxygen species (ROS). Deleting CypD protected against these sevoflurane-induced effects, highlighting CypD
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- Repeated exposure to anesthesia in early life may lead to cognitive impairment.
- Sevoflurane affects neurogenesis and cognitive function by altering mitochondrial function and cyclophilin D (CypD) levels.
- Neural progenitor cell (NPC) migration is crucial for cognitive development, but its regulation by sevoflurane via CypD is unknown.
Purpose of the Study:
- To investigate whether sevoflurane regulates neural progenitor cell (NPC) migration through alterations in cyclophilin D (CypD).
- To determine the role of CypD in sevoflurane-induced effects on NPC migration and associated molecular changes.
Main Methods:
- Neural progenitor cells (NPCs) and young mice from wild-type (WT) and CypD knockout (KO) models were exposed to sevoflurane.
- Immunofluorescence staining, wound healing assays, Transwell assays, mass spectrometry, and Western blot analyses were employed.
- Levels of CypD, reactive oxygen species (ROS), and doublecortin were assessed, alongside NPC migration.
Main Results:
- Sevoflurane exposure increased CypD and ROS levels while decreasing doublecortin and NPC migration in WT mice.
- These sevoflurane-induced impairments were significantly attenuated in CypD knockout (KO) mice.
- The results indicate that sevoflurane's negative impact on NPC migration is dependent on the presence of CypD.
Conclusions:
- Sevoflurane anesthesia impairs neural progenitor cell (NPC) migration in a CypD-dependent manner.
- This study establishes a mechanistic link between sevoflurane exposure, CypD, and impaired NPC migration.
- Findings provide a foundation for further research into anesthesia-related cognitive risks in developing brains.
Abstract:
Clinical studies have suggested that repeated exposure to anesthesia and surgery at a young age may increase the risk of cognitive impairment. Our previous research has shown that sevoflurane can affect neurogenesis and cognitive function in young animals by altering cyclophilin D (CypD) levels and mitochondrial function. Neural progenitor cells (NPCs) migration is associated with cognitive function in developing brains. However, it is unclear whether sevoflurane can regulate NPCs migration via changes in CypD. To address this question, we treated NPCs harvested from wild-type (WT) and CypD knockout (KO) mice and young WT and CypD KO mice with sevoflurane. We used immunofluorescence staining, wound healing assay, transwell assay, mass spectrometry, and Western blot to assess the effects of sevoflurane on CypD, reactive oxygen species (ROS), doublecortin levels, and NPCs migration. We showed that sevoflurane increased levels of CypD and ROS, decreased levels of doublecortin, and reduced migration of NPCs harvested from WT mice in vitro and in WT young mice. KO of CypD attenuated these effects, suggesting that a sevoflurane-induced decrease in NPCs migration is dependent on CypD. Our findings have established a system for future studies aimed at exploring the impacts of sevoflurane anesthesia on the impairment of NPCs migration.
