Abstract:
:The commonly used volatile anesthetic sevoflurane has been shown to induce widespread apoptosis in the developing brain, yet the underlying molecular mechanisms are not fully understood. Accumulating research has demonstrated that long noncoding RNAs (lncRNAs) regulate multiple biological processes, including neural development, differentiation and apoptosis. They are aberrantly expressed in multiple neurodegenerative diseases. In this study, we employed a lncRNA-mRNA microarray analysis to determine whether and how lncRNAs are involved in sevoflurane-induced hippocampal neuronal apoptosis in neonatal mice. Our data showed that a single 6-h sevoflurane exposure of P7 mice resulted in significant morphological changes and apoptosis in the hippocampus. Moreover, the microarray simultaneously revealed 817 lncRNAs and 856 of their potential coding targets that related to apoptosis, of which 31 lncRNAs (19 up and 12 down) and 25 mRNAs were significantly differentially expressed (P < 0.05) after sevoflurane exposure. Importantly, we found that Bcl2l11 (BIM), which potentiates mitochondria-dependent apoptosis and its nearby enhancer-like lncRNA ENSMUST00000136025, were both more highly expressed in sevoflurane-treated samples compared with control samples. Subsequent qRT-PCR results confirmed the changes. Further CNC network indicated that lncRNA ENSMUST00000136025 was positively correlated with Bim. Moreover, sevoflurane induced a significant increase of pro-apoptotic protein BIM and Bax but a reduction of anti-apoptotic proteins Bcl-2 in the hippocampus. Our study first demonstrates that aberrantly expressed lncRNAs play a role in sevoflurane-induced hippocampal apoptosis. We noted that up-regulated ENSMUST00000136025 highly likely induced the over-expression of BIM, which eventually promoted mitochondria-mediated apoptosis. Such findings further broaden the understanding of molecular mechanisms responsible for sevoflurane-induced neurotoxicity.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Chen X,Zhou X,Lu D,Yang X,Zhou Z,Chen X,Chen Y,He W,Feng Xdoi
10.1007/s11011-016-9838-6subject
Has Abstractpub_date
2016-10-01 00:00:00pages
1031-40issue
5eissn
0885-7490issn
1573-7365pii
10.1007/s11011-016-9838-6journal_volume
31pub_type
杂志文章abstract::Stroke is devastating and a leading cause of morbidity and mortality worldwide. Cerebral ischemia-reperfusion and its subsequent reactive hyperemia lead to neuronal damage in the hippocampus and cognitive decline. Chrysin (5, 7-dihydroxyflavone) is a well-known member of the flavonoid family with antioxidant and neuro...
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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更新日期:2015-10-01 00:00:00
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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