Hypoxic Preconditioning: A Novel Intrinsic Cytoprotective Strategy

Lu, Guowei; Yu, Shun; Li, Rao-Hua; Cui, Xiuyu; Gao, Chong

doi:10.1385/mn:31:1-3:255

Cited by 48 publications

(37 citation statements)

References 41 publications

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“…With each additional run of hypoxia we noted that the animal’s tolerance increased. Tolerance time in runs 2, 3, 4, and 5 was approximately 2, 4, 6, and 8 times greater, respectively, than times observed in the first run (Lu et al, 1999, 2005). This demonstrates HPC’s protective role.…”

Section: Hypoxic Preconditioning (Hpc): History and Neuroprotectivmentioning

confidence: 69%

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Preconditioning in neuroprotection: From hypoxia to ischemia

Hafeez

Noorulla

et al. 2017

Progress in Neurobiology

174

114

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Sublethal hypoxic or ischemic events can improve the tolerance of tissues, organs, and even organisms from subsequent lethal injury caused by hypoxia or ischemia. This phenomenon has been termed hypoxic or ischemic preconditioning (HPC or IPC) and is well established in the heart and the brain. This review aims to discuss HPC and IPC with respect to their historical development and advancements in our understanding of the neurochemical basis for their neuroprotective role. Through decades of collaborative research and studies of HPC and IPC in other organ systems, our understanding of HPC and IPC-induced neuroprotection has expanded to include: early- (phosphorylation targets, transporter regulation, interfering RNA) and late- (regulation of genes like EPO, VEGF, and iNOS) phase changes, regulators of programmed cell death, members of metabolic pathways, receptor modulators, and many other novel targets. The rapid acceleration in our understanding of HPC and IPC will help facilitate transition into the clinical setting.

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Section: Hypoxic Preconditioning (Hpc): History and Neuroprotectivmentioning

confidence: 69%

“…This occurs primarily at the cellular level and is discussed in detail below. Of clinical significance, the mechanisms underlying plasticity and modulation can point to novel strategies for the prevention and treatment of hypoxic and ischemic injury (Lu et al, 1999, 2005; Wang et al, 2007). …”

Section: Introductionmentioning

confidence: 99%

Preconditioning in neuroprotection: From hypoxia to ischemia

Hafeez

Noorulla

et al. 2017

Progress in Neurobiology

174

114

View full text Add to dashboard Cite

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“…In WbHPC animals, the internal state seems to fluctuate to conform to the available oxygen challenge in the environment in terms of energy conservation (manuscript in preparation), brain plasticity, and antihypoxia factor/gene activation [39][40][41][42][43] (Fig. 1).…”

Section: Mechanisms and Implications Of Hpcmentioning

confidence: 99%

Hypoxic preconditioning in an autohypoxic animal model

Shao

2012

Neurosci. Bull.

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Abstract:Hypoxic preconditioning refers to the exposure of organisms, systems, organs, tissues or cells to moderate hypoxia/ischemia that results in increased resistance to a subsequent episode of severe hypoxia/ischemia. In this article, we review recent research based on a mouse model of repeated exposure to autohypoxia. Pre-exposure markedly increases the tolerance to or protection against hypoxic insult, and preserves the cellular structure of the brain. Furthermore, the hippocampal activity amplitude and frequency of electroencephalogram, latency of cortical somatosensory-evoked potential and spinal somatosensory-evoked potential progressively decrease, while spatial learning and memory improve. In the brain, detrimental neurochemicals such as free radicals are down-regulated, while beneficial ones such as adenosine are upregulated. Also, antihypoxia factor(s) and gene(s) are activated. We propose that the tolerance and protective effects depend on energy conservation and plasticity triggered by exposure to hypoxia via oxygen-sensing transduction pathways and hypoxia-inducible factor-initiated cascades. A potential path for further research is the development of devices and pharmaceuticals acting on antihypoxia factor(s) and gene(s) for the prevention and treatment of hypoxia and related syndromes.

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“…Hence, cobalt can be used to mimic hypoxia to increase HIF-α [17,19]. We have proposed that HIF-1α can play a center role in the tolerance time in autoprogressive hypoxic mice [20]. However, Vangeison et al reported that loss of HIF-1α function in neurons reduced neuronal viability during hypoxia.…”

Section: Introductionmentioning

confidence: 99%

The Effects of CoCl2 on HIF-1α Protein under Experimental Conditions of Autoprogressive Hypoxia Using Mouse Models

Zhang

Wang

Meister

et al. 2014

IJMS

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It is well known that cobalt chloride (CoCl2) can enhance the stability of hypoxia-inducible factor (HIF)-1α. The aim of this study is to detect the effect of CoCl2 on the hypoxia tolerance of mice which were repeatedly exposed to autoprogressive hypoxia. Balb/c mice were randomly divided into groups of chemical pretreatment and normal saline (NS), respectively injected with CoCl2 and NS 3 h before exposure to hypoxia for 0 run (H0), 1 run (H1), and 4 runs (H4). Western Blot, electrophoretic mobility shift assay (EMSA), extracellular recordings population spikes in area cornus ammonis I (CA 1) of mouse hippocampal slices and real-time were used in this study. Our results demonstrated that the tolerance of mice to hypoxia, the changes of HIF-1α protein level and HIF-1 DNA binding activity in mice hippocampus, the mRNA level of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), and the disappearance time of population spikes of hippocampal slices were substantially different between the control group and the CoCl2 group. Over-induction of HIF-1α by pretreatment with CoCl2 before hypoxia did not increase the hypoxia tolerance.

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Hypoxic Preconditioning: A Novel Intrinsic Cytoprotective Strategy

Cited by 48 publications

References 41 publications

Preconditioning in neuroprotection: From hypoxia to ischemia

Preconditioning in neuroprotection: From hypoxia to ischemia

Hypoxic preconditioning in an autohypoxic animal model

The Effects of CoCl2 on HIF-1α Protein under Experimental Conditions of Autoprogressive Hypoxia Using Mouse Models

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