| Literature DB >> 27796156 |
Qiliang Jiang1, Yingwei Wang2, Xueyin Shi1.
Abstract
Prolonged or high-dose exposure to anesthetics, such as propofol, can cause brain cell degeneration and subsequent long-term learning or memory deficits, particularly in the developing brain. However, the cellular and molecular mechanisms underlying the deleterious effects of propofol at certain stages of development remain unclear. In this study we found that propofol inhibited the proliferation, neuronal differentiation, and migration of neural stem cells (NSCs) while upregulating miR-141-3p. Silencing of miR-141-3p abrogated the effects of propofol on NSC neurogenesis. Propofol treatment downregulated IGF2BP2, a direct target of miR-141-3p, whereas overexpression of IGF2BP2 attenuated the effects of propofol and miR-141-3p on NSC neurogenesis. In short, propofol inhibits NSC neurogenesis through a mechanism involving the miR-141-3p/IGF2BP2 axis. Our results may provide a potential approach for preventing the neurodegenerative effects of propofol in the developing brain.Entities:
Keywords: IGF2BP2; microRNA-141-3p; neural stem cell; neurogenesis; propofol
Mesh:
Substances:
Year: 2016 PMID: 27796156 DOI: 10.1089/scd.2016.0257
Source DB: PubMed Journal: Stem Cells Dev ISSN: 1547-3287 Impact factor: 3.272