Increased Phosphorylation of Ets-like Transcription Factor-1 in Neurons of Hypoxic Preconditioned Mice

Jiang, Jun; Yang, Weiwei; Huang, Ping; Bu, Xiangning; Zhang, Nan; Li, Junfa

doi:10.1007/s11064-009-9931-x

Cited by 11 publications

(4 citation statements)

References 32 publications

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“…and Neurochem Res (2012) 37:49-58 51 perfused transcardially with 0.9% NaCl, followed by 4% paraformaldehyde as our previous reports [33]. The brains were removed, postfixed in 4% paraformaldehyde for 24 h, and dehydrated in 30% sucrose solution.…”

Section: Double-labeled Immunofluorescent Stainingmentioning

confidence: 99%

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Luo-wa

Han

et al. 2011

Neurochem Res

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Propofol and ketamine may provide certain degree of neuroprotection, but the underlying mechanism remains unclear to date. The cAMP response element-binding protein (CREB) was proposed that its phosphorylation at Ser133 (P-CREB) constituted a convergence point involved in neuroprotection. The purpose of this study was to determine whether different dosages of propofol and ketamine could provide neuroprotection against permanent middle cerebral artery occlusion (MCAO)-induced ischemic injuries and the involvement of P-CREB. Eighty adult male BALB/c mice that underwent 6 h MCAO were randomly divided into eight groups: Sham-operation; MCAO + saline; MCAO + 25, 50, 100 mg/kg propofol; and MCAO + 25, 50, 100 mg/kg ketamine (intraperitoneal injection 30 min following MCAO). We found that 50, 100 (not 25) mg/kg propofol, and 25 (not 50 and 100) mg/kg ketamine could significantly reduce the infarct volume, edema ratio and neurological deficit (n = 10 per group) as well as inhibit the decrease of P-CREB level in peri-infarct region when compared with that of MCAO + saline group (n = 6 per group). In addition, the results of double-labeled immunofluorescent staining showed that P-CREB co-localized with neuron-specific marker, NeuN, in the peri-infarct region of 50 mg/kg propofol and 25 mg/kg ketamine treated 6 h MCAO mice (n = 4 per group). These results suggested that inhibition of neuron-specific P-CREB dephosphorylation in the peri-infarct region is involved in high dose propofol and low dose ketamine-induced neuroprotection of 6 h MCAO mice.

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Section: Double-labeled Immunofluorescent Stainingmentioning

confidence: 99%

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Luo-wa

Han

et al. 2011

Neurochem Res

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“…Elk4 has been investigated to be a target of MAPK and be a key role in neuronal differentiation, proliferation, and apoptosis after hypoxic injury (Jiang et al . ). Tgfb2, which is regulated by another target gene Rras2 (Patmore et al .…”

Section: Discussionmentioning

confidence: 97%

Analysis of long non‐coding RNA expression profiles in neonatal rats with hypoxic‐ischemic brain damage

Zhou

Wang

Cheng

et al. 2019

Journal of Neurochemistry

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Hypoxic-ischemic brain damage (HIBD) which is a common cause of acute mortality and neurological dysfunction in neonates still lacks effective therapeutic methods. Long noncoding RNAs (lncRNAs) were demonstrated to play a crucial role in many diseases. To give a foundation for subsequent functional studies of lncRNAs in HIBD, we investigated the profiling of lncRNAs and messenger RNAs (mRNAs) using neonatal HIBD rat model. Six neonatal rats were divided into sham-operated group (n = 3) and HIBD group (n = 3) randomly. Deep RNA sequencing was implemented to find out the meaningful lncRNAs and mRNAs. Quantitative realtime PCR was used to validate expressions of lncRNAs and mRNAs. The Gene Ontology (GO) and kyoto encyclopedia of genes a genomes (KEGG) database were used to predict functions of lncRNAs. A total of 328 differentially expressed lncRNAs (177 down-regulated vs 151 up-regulated) and 7157 differentially expressed mRNAs (2552 down-regulated vs 4605 up-regulated) were identified. The Quantitative realtime PCR results showed significant differential expressions of five lncRNAs and five mRNAs which were consistent with the RNA-Seq data. Gene ontology and KEGG analysis showed these lncRNAs and their expression-correlated mRNAs were closely related to the Janus tyrosine kinasesignal transducer and activator of transcription (JAK-STAT) signaling pathway, NF-kappa B signaling pathway, Toll-like receptor signaling pathway, calcium signaling pathway, Notch signaling pathway, mitogen activated protein kinase signaling pathway, neuroactive ligand-receptor interaction pathway and more. The results of our study identified the characterization and expression profiles of lncRNAs in neonatal HIBD and may be a basis for further therapeutic research.

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“…Hypoxic preconditioning (HP) is an exogenous phenomenon in which brief episodes of a hypoxic sublethal insult induces protection against the deleterious effects of subsequent lethal anoxia or ischemia [39,87]. The brain is one of the first organs to fail in hypoxia due to its high intrinsic rate of oxygen consumption.…”

Section: The Vital Role Of Hif-1 In Hpmentioning

confidence: 99%

The Protective Role of Hypoxic Preconditioning in CNS

Wu¹,

Zhu²,

Fan³

2012

Anoxia

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Increased Phosphorylation of Ets-like Transcription Factor-1 in Neurons of Hypoxic Preconditioned Mice

Cited by 11 publications

References 32 publications

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Inhibition of Neuron-Specific CREB Dephosphorylation is Involved in Propofol and Ketamine-Induced Neuroprotection Against Cerebral Ischemic Injuries of Mice

Analysis of long non‐coding RNA expression profiles in neonatal rats with hypoxic‐ischemic brain damage

The Protective Role of Hypoxic Preconditioning in CNS

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