Mild preconditioning hypoxia modifies nerve growth factor-induced gene A messenger RNA expression in the rat brain induced by severe hypoxia

Рыбникова, Е. А.; Tulkova, Ekaterina; Pelto‐Huikko, Markku; Самойлов, М. О.

doi:10.1016/s0304-3940(02)00577-3

Cited by 30 publications

(7 citation statements)

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“…At the same time, the survival of preconditioned rats during severe hypoxia reached 80%, and the quantity of injured and dead neurons in all brain structures studied was substantially decreased (Rybnikova et al, 2004). The ameliorating effects of preconditioning on rat behavior and expression of immediate early genes (Samoilov et al, 2001; Rybnikova et al, 2002) and proteins (Rybnikova et al, 2004) after severe hypoxia have been shown in the same model.…”

Section: Discussionmentioning

confidence: 93%

“…It has been demonstrated that a preconditioning with repetitive episodes of mild hypoxia/ischemia increases structural and functional neuronal resistance to subsequent severe hypoxia/ischemia (Kitagawa et al, 1990; Corbett and Crooks, 1997; Qi et al, 2001; Romanovskii et al, 2001; Wu et al, 2001; Rybnikova et al, 2002; Semenov et al, 2002; Samoilov et al, 2003). The ischemia‐induced cytochrome c release from mitochondria in the hippocampal CA1 region was suppressed after 5 min of ischemic preconditioning in gerbils (Nakatsuka et al, 2000).…”

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confidence: 99%

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Preconditioning enhances the expression of mitochondrial antioxidant thioredoxin‐2 in the forebrain of rats exposed to severe hypobaric hypoxia

Stroev

Gluschenko

Tjulkova

et al. 2004

J of Neuroscience Research

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The impact of severe hypoxia and preconditioning on the expression of the mitochondrial antioxidant thioredoxin-2 (Trx-2) in rat hippocampus (CA1, CA2, CA3 fields, and dentate gyrus) and neocortex was studied by immunocytochemistry. The preconditioning consisted of three trials of mild hypobaric hypoxia (360 Torr, 2 hr) spaced at 24 hr. The last trial was followed by severe hypobaric hypoxia (180 Torr, 3 hr) 24 hr later. Both in hippocampus and in neocortex, severe hypobaric hypoxia resulted in enhanced Trx-2 expression at 3 hr, followed by a slight decline in Trx-2 levels, which nevertheless remained increased at 24 hr elsewhere except for the CA1 region. The preconditioning considerably augmented severe hypoxia-induced Trx-2 immunoreactivity, affecting both the number of immunoreactive cells and the intensity of immunostaining. The findings suggest a role for Trx-2 in the formation of brain hypoxic/ischemic tolerance accomplished by the preconditioning.

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Section: Discussionmentioning

confidence: 93%

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confidence: 99%

Preconditioning enhances the expression of mitochondrial antioxidant thioredoxin‐2 in the forebrain of rats exposed to severe hypobaric hypoxia

Stroev

Gluschenko

Tjulkova

et al. 2004

J of Neuroscience Research

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“…These, in particular, include immediate early genes c‐fos and zif268 (NGFI‐A) , genes of peptide antioxidants, neurotrophins, and anti‐apoptotic gene superfamily bcl‐2 . We have previously shown that in mild hypoxia preconditioned rats, in contrast to non‐preconditioned ones, the modifications of immediate early gene activity followed by increased expression of NGFI‐A and c‐ Fos proteins, enhancement of cytosolic and mitochondrial antioxidant expression (Trx‐1, Cu, Zn‐SOD, Trx‐2, Mn‐SOD), up‐regulation of levels of anti‐apoptotic proteins Bcl‐2 and Bcl‐xL and down‐regulation of pro‐apoptotic protein Bax levels in the neocortex and hippocampus in response to severe hypoxia (Rybnikova et al. 2002, 2005a,b, 2006; Stroev et al.…”

Section: Discussionmentioning

confidence: 99%

“…2005a,b, 2006). It was also revealed that preconditioning modified the expression of proteins – products of immediate early genes zif‐268 and c‐fos , antioxidants of thioredoxin and superoxid dismutase families, mitogen‐activated protein‐kinases ERK, JNK1/2 and p38, apoptosis‐related factors of bcl‐2 superfamily in hippocampus and neocortex in response to severe hypoxia (Rybnikova et al. 2002, 2005a,b, 2006; Stroev et al.…”

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confidence: 99%

Preconditioning induces prolonged expression of transcription factors pCREB and NF‐κB in the neocortex of rats before and following severe hypobaric hypoxia

Рыбникова

Gluschenko

Tulkova

et al. 2008

Journal of Neurochemistry

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Preconditioning using mild repetitive hypobaric hypoxia is known to increase a tolerance of brain neurons to severe hypoxia and other injurious exposures. In the present study, the effects of mild hypoxic preconditioning on the expression of transcription factors NF-jB and phosphorylated CREB (pCREB) has been studied in the neocortex of rats exposed to severe hypobaric hypoxia. As revealed by quantitative immunocytochemistry, the injurious severe hypobaric hypoxia (180 Torr, 3 h) remarkably reduced the neocortical levels of pCREB and NF-jB. The three-trial hypoxic preconditioning (360 Torr, 2 h, 3 days) induced persistent up-regulation of pCREB and NF-jB expression in the neocortex of rats 3-24 h following the severe hypoxia. In addition, the preconditioning alone which was not followed by the severe hypoxia, considerably increased neocortical pCREB and NF-jB levels. The findings suggest a role for transcription factors cAMP response element-binding protein and NF-jB in the neuroprotective mechanisms activated by the hypoxic preconditioning.

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“…As examples, an ischemic preconditioning upregulates transcription of NGF and BDNF (Truettner et al, 2002;Matsushima et al, 1998) and produces a reinforcing effect on the transcription factor HIF-1 accumulation during a subsequent hypoxic injury (Giusti and Fiszer de Plazas, 2012). It was also shown that a mild hypobaric hypoxia preconditioning induces persistent upregulation of various transcription factors (c-Fos, NGFI-A, pCREB, NF-kB) both before and after a severe hypoxic event (Rybnikova et al, 2002(Rybnikova et al, , 2009. It is interesting mentioning that, in the field of medicine, experimental and clinical studies have shown that NGF up-regulation plays a pivotal role in protecting neurons against ischemia (Lindvall et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

NGF, TrkA‐P and neuroprotection after a hypoxic event in the developing central nervous system

Bogetti

Devoto

Rapacioli

et al. 2018

Intl J of Devlp Neuroscience

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A decrease in the concentration of oxygen in the blood and tissues (hypoxia) produces important, sometimes irreversible, damages in the central nervous system (CNS) both during development and also postnatally. The present work aims at analyzing the expression of nerve growth factor (NGF) and p75 and the activation of TrkA in response to an acute normobaric hypoxic event and to evaluate the possible protective role of exogenous NGF. The developing chick optic tectum (OT), a recognized model of corticogenesis, was used as experimental system by means of in vivo and in vitro studies. Based on identification of the period of highest sensitivity of developmental programmed cell death (ED15) we show that hypoxia has a mild but reproducible effect that consist of a temporal increase of cell death 6 h after the end of a hypoxic treatment. Cell death was preceded by a significant early increase in the expression of Nerve Growth Factor (NGF) and its membrane receptor p75. In addition, we found a biphasic response of TrkA activation: a decrease during hypoxia followed by an increase -4 h later- that temporally coincide with the interval of NGF overexpression. To test the NGF - NGF receptors role in hypoxic cell death, we quantified, in primary neuronal cultures derived from ED15 OT, the levels of TrkA activation after an acute hypoxic treatment. A significant decline in the level of TrkA activation was observed during hypoxia followed, 24 h later, by significant cell death. Interestingly, this cell death can be reverted if TrkA inactivation during hypoxia is suppressed by the addition of NGF. Our results suggest that TrkA activation may play an important role in the survival of OT neurons subjected to acute hypoxia. The role of TrkA in neuronal survival after injury may be advantageously used for the generation of neuroprotective strategies to improve prenatal insult outcomes.

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Mild preconditioning hypoxia modifies nerve growth factor-induced gene A messenger RNA expression in the rat brain induced by severe hypoxia

Cited by 30 publications

References 20 publications

Preconditioning enhances the expression of mitochondrial antioxidant thioredoxin‐2 in the forebrain of rats exposed to severe hypobaric hypoxia

Preconditioning enhances the expression of mitochondrial antioxidant thioredoxin‐2 in the forebrain of rats exposed to severe hypobaric hypoxia

Preconditioning induces prolonged expression of transcription factors pCREB and NF‐κB in the neocortex of rats before and following severe hypobaric hypoxia

NGF, TrkA‐P and neuroprotection after a hypoxic event in the developing central nervous system

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