Neuroprotection of brain‐derived neurotrophic factor against hypoxic injury <i>in vitro</i> requires activation of extracellular signal‐regulated kinase and phosphatidylinositol 3‐kinase

Sun, Xiaomei; Zhou, Huaiyu; Luo, Xiaorong; Li, Shengfu; Yu, Dan; Jiping, Hua; Mu, Dezhi; Mao, Meng

doi:10.1016/j.ijdevneu.2007.11.005

Cited by 38 publications

(40 citation statements)

References 30 publications

(55 reference statements)

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“…Moreover, Haraguchi et al (2011) reported that estradiol promotes Purkinje dendritic growth, spinogenesis, and synaptogenesis during neonatal life by inducing the expression of BDNF . BDNF protects against hypoxic injury by activating PI3K/Akt signaling (Sun et al, 2008). These observations indicate that 17β-estradiolmediated signaling cross talks with the intracellular signaling mediated by BDNF.…”

Section: Discussionmentioning

confidence: 69%

17β-estradiol attenuates ketamine-induced neuroapoptosis and persistent cognitive deficits in the developing brain

Wang

et al. 2014

Brain Research

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Section: Discussionmentioning

confidence: 69%

17β-estradiol attenuates ketamine-induced neuroapoptosis and persistent cognitive deficits in the developing brain

Wang

et al. 2014

Brain Research

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“…Numerous experimental studies have indicated the effectiveness of BDNF against various brain pathologies, including hypoxic states [10,47,48] and neurodegenerative diseases [4,15,16,17,18,19,20,21]. Therefore, this neurotrophin could be considered a potential therapeutic agent for some of the most comprehensive pathologies associated with death and patient disability.…”

Section: Discussionmentioning

confidence: 99%

AAV-Syn-BDNF-EGFP Virus Construct Exerts Neuroprotective Action on the Hippocampal Neural Network during Hypoxia In Vitro

Митрошина

Mishchenko

Usenko

et al. 2018

IJMS

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Brain-derived neurotrophic factor (BDNF) is one of the key signaling molecules that supports the viability of neural cells in various brain pathologies, and can be considered a potential therapeutic agent. However, several methodological difficulties, such as overcoming the blood–brain barrier and the short half-life period, challenge the potential use of BDNF in clinical practice. Gene therapy could overcome these limitations. Investigating the influence of viral vectors on the neural network level is of particular interest because viral overexpression affects different aspects of cell metabolism and interactions between neurons. The present work aimed to investigate the influence of the adeno-associated virus (AAV)-Syn-BDNF-EGFP virus construct on neural network activity parameters in an acute hypobaric hypoxia model in vitro. Materials and methods. An adeno-associated virus vector carrying the BDNF gene was constructed using the following plasmids: AAV-Syn-EGFP, pDP5, DJvector, and pHelper. The developed virus vector was then tested on primary hippocampal cultures obtained from C57BL/6 mouse embryos (E18). Acute hypobaric hypoxia was induced on day 21 in vitro. Spontaneous bioelectrical and calcium activity of neural networks in primary cultures and viability tests were analysed during normoxia and during the posthypoxic period. Results. BDNF overexpression by AAV-Syn-BDNF-EGFP does not affect cell viability or the main parameters of spontaneous bioelectrical activity in normoxia. Application of the developed virus construct partially eliminates the negative hypoxic consequences by preserving cell viability and maintaining spontaneous bioelectrical activity in the cultures. Moreover, the internal functional structure, including the activation pattern of network bursts, the number of hubs, and the number of connections within network elements, is also partially preserved. BDNF overexpression prevents a decrease in the number of cells exhibiting calcium activity and maintains the frequency of calcium oscillations. Conclusion. This study revealed the pronounced antihypoxic and neuroprotective effects of AAV-Syn-BDNF-EGFP virus transduction in an acute normobaric hypoxia model.

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“…Both in vivo and in vitro studies have demonstrated BDNF-induced neuroprotection against hypoglycemia, ischemia, and hypoxia [108, 109]. Since DOR is highly expressed in cortical and striatal regions [20, 21], we further investigated if DOR protects them from hypoxic injury through BDNF [110].…”

Section: Dor Neuroprotection Via Bdnf-trkb Pathwaymentioning

confidence: 99%

Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

Sheng¹,

Huang²,

Ren³

et al. 2018

Cell Physiol Biochem

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The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR’s role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain, we clarified DOR’s specific role in the brain against hypoxic/ischemic injury and reconciled previous controversies in this aspect. Our serial studies have strongly demonstrated that DOR is a unique neuroprotector against hypoxic/ischemic injury in the brain, which has been well confirmed in current research. Moreover, mechanistic studies have shown that during acute phases of hypoxic/ischemic stress, DOR protects the neurons mainly by the stabilization of ionic homeostasis, inhibition of excitatory transmitter release, and attenuation of disrupted neuronal transmission. During prolonged hypoxia/ischemia, however, DOR neuroprotection involves a variety of signaling pathways. More recently, our data suggest that DOR may display its neuroprotective role via the BDNF-TrkB pathway. This review concisely summarizes the progress in this field.

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Neuroprotection of brain‐derived neurotrophic factor against hypoxic injury in vitro requires activation of extracellular signal‐regulated kinase and phosphatidylinositol 3‐kinase

Cited by 38 publications

References 30 publications

17β-estradiol attenuates ketamine-induced neuroapoptosis and persistent cognitive deficits in the developing brain

17β-estradiol attenuates ketamine-induced neuroapoptosis and persistent cognitive deficits in the developing brain

AAV-Syn-BDNF-EGFP Virus Construct Exerts Neuroprotective Action on the Hippocampal Neural Network during Hypoxia In Vitro

Neuroprotection Against Hypoxic/Ischemic Injury: δ-Opioid Receptors and BDNF-TrkB Pathway

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