ArticleJournal of anesthesia2017
Isoflurane decreases proliferation and differentiation, but none of the effects persist in human embryonic stem cell-derived neural progenitor cells.
Article in Journal of anesthesia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Subunit-specific mechanisms of isoflurane-induced acute tonic inhibition in dentate gyrus granule neuron.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Article
- Effects of short-term exposure to sevoflurane on the survival, proliferation, apoptosis, and differentiation of neural precursor cells derived from human embryonic stem cells.Journal of anesthesia · 2017Article
- Modulation of Neocortical Development by Early Neuronal Activity: Physiology and Pathophysiology.Frontiers in cellular neuroscience · 2017Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeVolatile anesthetics are a potential risk for cognitive impairment in the developing brain. Isoflurane causes cell death, reduces neurogenesis, and changes neuronal differentiation. In this study, the effects of a single isoflurane exposure on the developing human brain were evaluated using human embryonic stem cell (hESC)-derived neural progenitor cells (NPCs).
methodsMultipotent NPCs were derived from hESCs and randomly exposed to either 5 vol% isoflurane (4 h) or no isoflurane (control group). The cells were fixed after 1, 3, 5, and 7 days to evaluate differentiation using the ratio of β-III tubulin to nestin. Neuronal cell survival and proliferation were assessed using the WST-1 and bromodeoxyuridine (BrdU) cell proliferation assays, respectively. To evaluate the mechanism of isoflurane neurotoxicity, we added TAT-Pep5, a p75 neurotrophic receptor (p75
resultsIsoflurane had minimal or no effect on the cell survival of NPCs in vitro. Proliferation, assessed on the basis of BrdU incorporation, was inhibited in the isoflurane group on days 3 (p = 0.033) and 5 (p = 0.001). The ratios of β-III tubulin to nestin in the isoflurane group on days 1 and 3 were significantly lower (p = 0.004 and p = 0.029, respectively) than those in the control group. Anti-proliferative and differentiation-reducing effect did not persist. TAT-Pep5 pretreatment significantly blocked the isoflurane-mediated decrease in the β-III tubulin to nestin ratio (p = 0.012) on day 1.
conclusionExposing NPCs to isoflurane hampered proliferation and differentiation but not neuronal survival. Isoflurane may be a powerful neuronal modulator during the early developmental period, partly mediated by activation of p75
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