HIF repressors under chronic hypoxia

Luo, Weibo; Wang, Yingfei

doi:10.18632/aging.100922

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…In this study, CIRBP over-expression significantly decreased the level of HIF-1α and the ratio of apoptosis in the 1% hypoxia exposed SH-SY5Y cells, indicating that over-expressing CIRBP could suppress HIF-1α expression and alleviate the hypoxia induced apoptosis. Recently, Weibo Luo et al reported several HIF repressors under chronic hypoxia 53 . They found several genes, such as peroxiredoxin 2 (PRDX2) and PRDX4, suppressed the level of HIF-1α mRNA and its transcriptional activity.…”

Section: Discussionmentioning

confidence: 99%

Cold Inducible RNA Binding Protein Is Involved in Chronic Hypoxia Induced Neuron Apoptosis by Down-Regulating HIF-1α Expression and Regulated By microRNA-23a

Chen

Liu

et al. 2017

Int. J. Biol. Sci.

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Background: Neuron apoptosis mediated by hypoxia inducible factor 1α (HIF-1α) in hippocampus is one of the most important factors accounting for the chronic hypobaric hypoxia induced cognitive impairment. As a neuroprotective molecule that is up-regulated in response to various environmental stress, CIRBP was reported to crosstalk with HIF-1α under cellular stress. However, its function under chronic hypobaric hypoxia remains unknown.Objective: In this study, we tried to identify the role of CIRBP in HIF-1α mediated neuron apoptosis under chronic hypobaric hypoxia and find a possible method to maintain its potential neuroprotective in long-term high altitude environmental exposure.Methods: We established a chronic hypobaric hypoxia rat model as well as a tissue culture model where SH-SY5Y cells were exposed to 1% hypoxia. Based on these models, we measured the expressions of HIF-1α and CIRBP under hypoxia exposure and examined the apoptosis of neurons by TUNEL immunofluorescence staining and western blot analysis of apoptosis related proteins. In addition, by establishing HIF-1α shRNA and pEGFP-CIRBP plasmid transfected cells, we confirmed the role of HIF-1α in chronic hypoxia induced neuron apoptosis and identified the influence of CIRBP over-expression upon HIF-1α and neuron apoptosis in the process of exposure. Furthermore, we measured the expression of the reported hypoxia related miRNAs in both models and the influence of miRNAs' over-expression/knock-down upon CIRBP in the process of HIF-1α mediated neuron apoptosis.Results: HIF-1α expression as well as neuron apoptosis was significantly elevated by chronic hypobaric hypoxia both in vivo and in vitro. CIRBP was induced in the early stage of exposure (3d/7d); however as the exposure was prolonged (21d), CIRBP level of the hypoxia group became significantly lower than that of control. In addition, HIF-1α knockdown significantly decreased neuron apoptosis under hypoxia, suggesting HIF-1α may be pro-apoptotic in the process of exposure. CIRBP over-expression significantly suppressed HIF-1α up-regulation in hypoxia and inhibited HIF-1α mediated neuron apoptosis. Interestingly, miR-23a was also induced by hypoxia exposure and showed the same changing tendency with CIRBP (increasing in 3d/7d, decreasing in 21d). In addition, over-expressing miR-23a up-regulated CIRBP, down-regulated HIF-1α and attenuated neuron apoptosis.Conclusion: Cold inducible RNA binding protein is involved in chronic hypoxia induced neuron apoptosis by down-regulating HIF-1α expression, and MiR-23a may be an important tool to maintain CIRBP level and function.

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Section: Discussionmentioning

confidence: 99%

Cold Inducible RNA Binding Protein Is Involved in Chronic Hypoxia Induced Neuron Apoptosis by Down-Regulating HIF-1α Expression and Regulated By microRNA-23a

Chen

Liu

et al. 2017

Int. J. Biol. Sci.

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“…In the present study, the overexpression of CIRP obviously decreased the HIF-1α level and the apoptotic rate of SH-SY5Y cells exposed to 1% O 2 , suggesting that the overexpression of CIRP can inhibit the HIF-1α expression and alleviate the hypoxia-induced apoptosis. Recently, Luo et al (18), reported several HIF inhibitors under chronic hypoxia, and found that several kinds of genes, such as peroxiredoxin 2 (PRDX2) and PRDX4, inhibit the HIF-1α mRNA level and transcriptional activity. Therefore, it is speculated that CIRP may repress HIF-1α during chronic hypobaric hypoxia-induced neuronal apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Association between CIRP expression and hypoxic‑ischemic brain injury in neonatal rats

2019

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The role of cold inducible RNA-binding protein (CIRP) in mediating ischemic brain injury in neonatal rats under chronic hypobaric hypoxia was investigated. The neonatal rat model of chronic hypobaric hypoxia and the cell culture model of SH-SY5Y cells exposed to hypoxia (1% O 2 ) were constructed. The expression of CIRP and hypoxia-inducible factor-1α (HIF-1α) was detected after hypoxic exposure, and the apoptosis-related proteins were analyzed via terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and western blot analysis to detect neuronal apoptosis. Moreover, the effects of CIRP overexpression on HIF-1α and neuronal apoptosis were identified. Chronic hypobaric hypoxia can lead to HIF-1α expression and neuronal apoptosis in the body. CIRP was induced at early exposure (3 d/7 d). However, the CIRP level in the hypoxic group was obviously lower than that in the control group with the prolongation of exposure time (21 d). In addition, the knockdown of HIF-1α significantly reduced the neuronal apoptosis under hypoxic conditions, indicating that HIF-1α may promote apoptosis during exposure. The overexpression of CIRP significantly inhibited the upregulation of HIF-1α during hypoxia and the HIF-1α-mediated neuronal apoptosis. Results of the current study showed that, CIRP is involved in the ischemic brain injury induced by chronic hypoxia through downregulation of HIF-1α expression.

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“…Важным фактором, влияющим на уровень эндотелина, является индуцированный гипоксией фактор (HIF-1α), который опосредует адаптивные механизмы при гипоксии и стимулирует синтез ЭТ-1. Установлено, что при хронической гипоксии происходит распад белка HIF-1α, что приводит к снижению уровня ЭТ-1 [3][4]. Можно предположить, что уровень ЭТ-1 может служить возможным показателем гипоксии, хотя это требует дальнейшего изучения.…”

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Endothelin-1 level in the tear fluid of children with primary congenital glaucoma

Катаргина

Сhesnokova

Arestova

et al. 2023

Rossijskij oftalʹmologičeskij žurnal

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Purpose. To analyze the level of endothelin-1 (ET-1) in the tear fluid (TF) of children with primary congenital glaucoma (PCG) and to detect possible correlations between the clinical and the laboratory data. Material and methods. We examined 23 eyes of 15 children with PCG aged between 7 months and 15 years and 3 healthy fellow eyes of these children. 25 eyes of children of same age without glaucoma (somatically healthy with mild hyperopia and/or concomitant strabismus) served as control. A standard ophthalmological examination was supplemented by the flash visual evoked cortical potential, a total and a rhythmic electroretinogram, axial length (AL) echobiometry of the eye, optical coherence tomography of the optic nerve head, enzyme immunoassay (ELISA) of ET-1 level in TF were given. Results. In most children with PCG (95.6 %), the TF level of ET-1 (mean 9.69 ± 3.80 pg/ml) was higher than that in healthy children (4.65 ± 2,02 pg/ml) (p < 0.001). Increased levels of ET-1 (up to 8.90 pg/ml) were also detected in healthy fellow eyes of children with PCG. The mean level of ET-1 in children with PCG aged 3 to 15 years was significantly higher (p< 0.05) lower than in the initial stage. Our study revealed no correlations between the ET-1 level and the degree of retinal nerve fiber layer thinning, or the AL in children with PCG. Conclusion. For the first time, an increased level of ET-1 in the TF in children with PCG was revealed as compared to healthy children. A lower value of ET-1 in the far advanced PCG stage as compared to the initial stage can be explained by long-term chronic eye tissue hypoxia depleting the protective reserves of the eye. Since no obvious correlation between ET-1 level in the TF and clinical and functional data of children with PVG has been found, we cannot definitely view the ET-1 level in the TF as a measure of ischemia degree in PCG. Further studies are needed to obtain reliable correlations.

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HIF repressors under chronic hypoxia

Cited by 3 publications

References 8 publications

Cold Inducible RNA Binding Protein Is Involved in Chronic Hypoxia Induced Neuron Apoptosis by Down-Regulating HIF-1α Expression and Regulated By microRNA-23a

Cold Inducible RNA Binding Protein Is Involved in Chronic Hypoxia Induced Neuron Apoptosis by Down-Regulating HIF-1α Expression and Regulated By microRNA-23a

Association between CIRP expression and hypoxic‑ischemic brain injury in neonatal rats

Endothelin-1 level in the tear fluid of children with primary congenital glaucoma

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