Hypoxic Adaptation in the Nervous System: Promise for Novel Therapeutics for Acute and Chronic Neurodegeneration

Speer, Rachel E.; Ratan, Rajiv R.

doi:10.1007/978-1-4899-7678-9_16

Cited by 14 publications

(12 citation statements)

References 115 publications

(92 reference statements)

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“…Thus, for the hypoxic preconditioning efficiency predicting and study of innate adaptive mechanisms, it is necessary to look for other, non-stressor methods for the separation of animals in their sensitivity to adaptive hypoxia. This will help to better understand the mechanisms of hypoxic preconditioning and to identify additional novel therapeutic targets for diverse acute and, possibly, chronic pathologies [13] [39].…”

Section: Hbh Effects On the Resistance To Shbh Of The Intact High Anmentioning

confidence: 99%

“…Hypoxic or ischaemic preconditioning in vitro and in vivo is a powerful protective mechanism against ischaemic injury and other acute injuries in many organ systems. Thus, the preconditioning effects were identified for the heart [1] [3] [4] [5], brain [6]- [13], liver [14] [15] [16] and kidneys [17] [18] in vivo.…”

Section: Introductionmentioning

confidence: 99%

“…Hypoxic/ischaemic preconditioning is a multifactorial process requiring the interaction of numerous signals, second messengers and effector mechanisms [8] [9] [12] [13] [19] [20] [21]. Understanding how to apply the hypoxic response to initiate the protective mechanism of ischemic preconditioning is a high priority [13]. Direct preconditioning action or the molecular effectors of the hypoxic protective response could reveal promising therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

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Hypoxic Preconditioning Eliminates Differences in the Innate Resistance of Rats to Severe Hypoxia

Захарова¹,

Dudchenko²

2016

JBiSE

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Hypoxic preconditioning is able to increase the body's resistance to hypoxic/ischemic stress. Understanding how to apply the hypoxic response to initiate the protective mechanism of ischemic preconditioning is a high priority. However, the relationship between innate resistance to hypoxic stress and preconditioning efficiency of moderate hypoxia has been poorly studied. In our work, the efficiency of single moderate hypobaric hypoxia (HBH) for resistance to severe hypobaric hypoxia (SHBH) was studied on intact rats and those pre-tested under SHBH with low, intermediate and high resistance to hypoxia. HBH has a significant preconditioning action on the resistance to hypoxia over a wide range from 270 to 1464 s (4.5 to 24.5 min) and at the same time eliminates the differences in the endurance under SHBH between all rat groups. It is concluded that 1) HBH preconditioning efficiency does not depend on an innate resistance to SHBH and prior hypoxic experience of rats; and 2) the pretesting to severe hypoxia has no value for predicting the hypoxic preconditioning efficiency and study of adaptive mechanisms.

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Section: Hbh Effects On the Resistance To Shbh Of The Intact High Anmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hypoxic Preconditioning Eliminates Differences in the Innate Resistance of Rats to Severe Hypoxia

Захарова¹,

Dudchenko²

2016

JBiSE

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“…Protection from hypoxic damage is also very relevant because the hypoxic component is involved in pathogenesis of many diseases. In vivo, protective action of the hypoxic or ischaemic preconditioning was identified in the diseases of brain [3,[10][11][12][13][14][15], heart [8,[16][17][18], liver [19][20][21] and kidneys [22,23]. Direct hypoxic preconditioning or drugs that mimic the hypoxic protective response could reveal promising therapeutic targets.…”

Section: Protective Action Of Moderate Hypoxiamentioning

confidence: 99%

Hypoxic Preconditioning: The Multiplicity of Central Neurotransmitter Mechanisms and Method of Predicting Its Efficiency

Захарова¹,

Storozheva²,

Proshin³

et al. 2018

Hypoxia and Anoxia

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In rats, a single moderate hypobaric hypoxia (HBH) increased the resistance to severe hypoxia (SHBH). The HBH efficiency and neurotransmitter mechanisms of its preconditioning action were investigated by biochemical and pharmacological methods. It will be substantiated in the chapter: (1) HBH preconditioning has its own mechanisms that do not depend on an innate resistance to SHBH and prior hypoxic experience of rats; (2) the same preconditioning effect can be achieved by diverse neuronal pathways and synaptic plasticity means; (3) cholinergic and, presumably, serotoninergic, GABAergic and/or glutamatergic systems of the caudal brainstem, cortex and some other brain structures are involved in HBH realisation; (4) the rate of sensorimotor gating estimated in the model of acoustic startle pre-pulse inhibition (PPI) predicts the efficiency of hypoxic preconditioning and (5) the cholinergic system, including α7 nicotinic receptors, is involved in the mechanisms of HBH-PPI-dependent preconditioning effects.

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“…HIF-1α regulates lots of genes involved in systemic, tissue and cellular adaption under low oxygen conditions [11] . It has been found that HIF-1α regulates hundreds of genes involved in adaption to low oxygen conditions including erythropoietin (EPO), vascular endothelial growth factor (VEGF), and several glycolytic enzymes, etc., which play crucial roles for neuroprotection and neurogenesis in the central nervous system [12,13] .…”

Section: Research Articlementioning

confidence: 99%

HIF-1α promotes NSCs migration by modulating Slit2-Robo1 signaling after cerebral ischemia

Ye¹,

Chen²,

2017

Receptor Clin Invest

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Our previous studies have shown that transplantation of Hypoxia-inducible factor-1α (HIF-1α) gene modified neural stem cells (NSCs) reduced brain injury by improving the survival of NSCs and protecting the vascular system. HIF-1α plays pivotal roles during hypoxia, and its downstream pathways might be the primary mechanisms for the growth of NSCs. However, there are very few studies reported whether HIF-1α regulates NSCs migration. In this study, to test the hypothesis that HIF-1α modulates migration of NSCs after cerebral ischemia, we compared the injection of HIF-1α gene recombinant adenovirus, and control adenovirus in ischemia penumbra at 24 h after transient middle cerebral artery occlusion (tMCAO). BrdU labeled NSCs were transplanted in the lateral ventricle at the same time in both groups. The modified neurological severity score (NSS) was used to evaluate neurological deficits. Immunohistochemistry for HIF-1α, BrdU, Slit2 and Robo1 were performed. Comparing with vehicle group HIF-1α group showed better behavioral recovery on day 21 and 28. Expression of HIF-1α in HIF-1α group is higher than that in vehicle group. In HIF-1α group, more BrdU-positive cells were found than that in vehicle group. There are increased Slit2 in HIF-1α group. However, robo1, a receptor of Slits is decreased than that in vehicle group. Thus, we concluded that in cerebral ischemia rat model HIF-1α increased NSCs migration by inhibiting Slit2-Robo1 pathway, and improved the neurological behavior. In conclusion, our results indicate that HIF-1α may be a potential therapeutic target for ischemic stroke through promoting neuroregeneration.

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Hypoxic Adaptation in the Nervous System: Promise for Novel Therapeutics for Acute and Chronic Neurodegeneration

Cited by 14 publications

References 115 publications

Hypoxic Preconditioning Eliminates Differences in the Innate Resistance of Rats to Severe Hypoxia

Hypoxic Preconditioning Eliminates Differences in the Innate Resistance of Rats to Severe Hypoxia

Hypoxic Preconditioning: The Multiplicity of Central Neurotransmitter Mechanisms and Method of Predicting Its Efficiency

HIF-1α promotes NSCs migration by modulating Slit2-Robo1 signaling after cerebral ischemia

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