Neuregulin-1 Protects Neuronal Cells Against Damage due to CoCl2-Induced Hypoxia by Suppressing Hypoxia-Inducible Factor-1α and P53 in SH-SY5Y Cells

Yoo, Seong-Yeon; Yoo, Ji Young; Kim, Han-Byeol; Baik, Tai-Kyoung; Lee, Jun-Ho; Woo, Ran-Sook

doi:10.5213/inj.1938190.095

Cited by 34 publications

(23 citation statements)

References 35 publications

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“…2d). These results are consistent with those of our previous studies demonstrating the effects of NRG1 on HIF-1α or p53 [23].…”

Section: Cocl 2 Increased Eaac1 Protein Expression In Sh-sy5y Cellssupporting

confidence: 94%

“…In this study, we showed that NRG1 could prevent CoCl 2 -induced upregulation of EAAC1 levels in SH-SY5Y cells. We also con rmed that NRG1 could attenuate the CoCl 2 -induced accumulation of HIF-1α and p53 [23].…”

Section: Discussionsupporting

confidence: 54%

“…NRG1 protects against a number of CNS pathological conditions, including ischemia, neurotrauma, and neurodegenerative diseases [18][19][20][21][22]. Our recent work showed that NRG1 regulated hypoxia-inducible factors such as HIF-1α and p53 [23]. NRG1/ErbB4 attenuates neuronal cell damage under OGD in primary hippocampal neurons [24].…”

Section: Introductionmentioning

confidence: 98%

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Neuregulin-1 Inhibits CoCl2-Induced Excitatory Amino Acid Carrier 1 Overexpression and Oxidative Stress in SH-SY5Y Cells

Kim

Yoo

et al. 2020

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Abstract Excitatory amino acid carrier 1 (EAAC1) is an important subtype of excitatory amino acid transporters (EAATs) and is the route for neuronal cysteine uptake. CoCl2 is not only a hypoxia-mimetic reagent but also an oxidative stress inducer. Here, we found that CoCl2 induced significant overexpression of EAAC1 in a dose- and time-dependent manner. We further demonstrated that pretreatment with NRG1 rescued the CoCl2-induced upregulation of EAAC1 and tau expression. Neuregulin-1 (NRG1) plays a protective role in the CoCl2-induced accumulation of reactive oxygen species (ROS) and reduction in antioxidative enzyme (SOD and Gpx) activity. Moreover, NRG1 attenuated CoCl2-induced apoptosis and cell death. NRG1 inhibited the CoCl2-induced release of cleaved caspase-3 and reduction in Bcl-XL. Our novel findings suggest that NRG1 may play a protective role in oxidative stress and hypoxia through the regulation of EAAC1.

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“…2d). These results are consistent with those of our previous studies demonstrating the effects of NRG1 on HIF-1α or p53 [23].…”

Section: Cocl 2 Increased Eaac1 Protein Expression In Sh-sy5y Cellssupporting

confidence: 94%

Section: Discussionsupporting

confidence: 54%

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Neuregulin-1 Inhibits CoCl2-Induced Excitatory Amino Acid Carrier 1 Overexpression and Oxidative Stress in SH-SY5Y Cells

Kim

Yoo

et al. 2020

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“…Because of the changes of autophagy activity, it is necessary to evaluate the autophagic flow as following: the dynamic changes of autophagosome formation, fusion of autophagosome and lysosome, substrate degradation, and so on [50]. CoCl 2 has been used as a chemical compound to simulate hypoxia in vivo and in vitro [51]. At present, we confirm that GAS reduced CoCl 2 -induced autophagic flux inhibition and the formation of autophagosomes vi apromoting lysosomal acidification and autophagosome-lysosome fusionin in HT22 cells.…”

Section: Discussionmentioning

confidence: 99%

Protection effect of gastrodin on learning and memory ability in vascular dementia by promoting autophagy flux via Ca2+/CaMKII signal pathway

Tt¹,

Zhou²,

Yn³

et al. 2020

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Background: Vascular dementia is a common and frequently-occurring disease in the process of human aging. Although the current treatment can delay the deterioration of the disease, it has not a great breakthrough in improving cognitive impairment. Therefore, exploring the potential key molecular targets of VD provide promising strategy for prevention and treatment. Methods: vascular dementia rats were reproduced by permanent middle cerebral artery occlusion (pMCAO) and anoxic injury of HT22 cells were induced by Cobalt Chloride (CoCl 2 , 200μM). The ability of spatial learning and memory was assessed by morris water maze (MWM) test. Histological analysis was performed by HE staining and immunohistochemical staining. The effects of gastrodin on autophagy flux and calcium signal in vascular dementia rats and HT22 cells during hypoxia injury were detected by Western blotting and immunofluorescence. Furthermore, intracellular Ca 2+ levels were quantified using a Ca 2+ quantification kit and were also measured by flow cytometric estimation of Fluo-4 AM. Results: Gastrodin significantly reversed cognitive deficits in vascular dementia rats. The results of immunohistochemical analysis and western blot confirmed that gastrodin could attenuate the levels of LC3, p62 and phosphorylated CaMKII in hippocampus of VD rats. In addition, gastrodin was similar to the early autophagic inhibitor (3-BDO) ameliorating CoCl 2 -induced autophagic flux dysfunction and p62 knockdown by siRNA also promoting autophagic flux patency, but the late autophagy inhibitor (CQ) weakened the improvement effect of gastrodin. Furthermore, gastrodin markedly inhibited CoCl 2 -induced autophagic flux dysfunction by inhibiting [Ca 2+ ] i -dependent CaMKII. Conclusion: Gastrodin is a potential promising candidate for VD by improving autophagy flux dysfunction via increasing lysosome acidification and autophagosome-lysosome fusion mediated by CaMKII-regulated suppression of p62 signaling. Keywords: Gastrodin, Vascular dementia, Neuron injury, Autophagic flux, Ca 2+ , CaMKII

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“…1b). CoCl 2 treatment signi cantly increased EAAC1 protein expression at each subsequent time point (0,1,3,6,12,24,36, and 48 hrs). EAAC1 protein expression was signi cantly increased after exposure to 100 μM CoCl 2 for > 24 hrs compared with that of the controls (n=6; *P<0.05, ***P<0.001;Fig.…”

mentioning

confidence: 99%

Neuregulin-1 inhibits CoCl2-induced upregulation of excitatory amino acid carrier 1 expression and oxidative stress in SH-SY5Y cells and the hippocampus of mice

Kim

Yoo

et al. 2020

Preprint

Self Cite

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Excitatory amino acid carrier 1 (EAAC1) is an important subtype of excitatory amino acid transporters (EAATs) and is the route for neuronal cysteine uptake. CoCl 2 is not only a hypoxia-mimetic reagent but also an oxidative stress inducer. Here, we found that CoCl 2 induced significant EAAC1 overexpression in SH-SY5Y cells and the hippocampus of mice. Transient transfection of EAAC1 reduced CoCl 2 -induced cytotoxicity in SH-SY5Y cells. Based on this result, upregulation of EAAC1 expression by CoCl 2 is thought to represent a compensatory response against oxidative stress in an acute hypoxic state. We further demonstrated that pretreatment with Neuregulin-1 (NRG1) rescued CoCl 2 -induced upregulation of EAAC1 and tau expression. NRG1 plays a protective role in the CoCl 2 -induced accumulation of reactive oxygen species (ROS) and reduction in antioxidative enzyme (SOD and GPx) activity. Moreover, NRG1 attenuated CoCl 2 -induced apoptosis and cell death. NRG1 inhibited the CoCl 2 -induced release of cleaved caspase-3 and reduction in Bcl-X L levels. Our novel finding suggests that NRG1 may play a protective role in hypoxia through the inhibition of oxidative stress and thereby maintain normal EAAC1 expression levels.

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Neuregulin-1 Protects Neuronal Cells Against Damage due to CoCl2-Induced Hypoxia by Suppressing Hypoxia-Inducible Factor-1α and P53 in SH-SY5Y Cells

Cited by 34 publications

References 35 publications

Neuregulin-1 Inhibits CoCl2-Induced Excitatory Amino Acid Carrier 1 Overexpression and Oxidative Stress in SH-SY5Y Cells

Neuregulin-1 Inhibits CoCl2-Induced Excitatory Amino Acid Carrier 1 Overexpression and Oxidative Stress in SH-SY5Y Cells

Protection effect of gastrodin on learning and memory ability in vascular dementia by promoting autophagy flux via Ca2+/CaMKII signal pathway

Neuregulin-1 inhibits CoCl2-induced upregulation of excitatory amino acid carrier 1 expression and oxidative stress in SH-SY5Y cells and the hippocampus of mice

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