Cited by 49Redox biology and oxidative stressNeurological Disorders and TreatmentsAntioxidant Activity and Oxidative Stress

Neural stem cells injured by oxidative stress can be rejuvenated by GV1001, a novel peptide, through scavenging free radicals and enhancing survival signals

Park, Hyun-Hee, Yu, Hyun-Jung, Kim, Sangjae, Kim, Gabseok, Choi, Na-Young, Lee, Eun-Hye, Lee, Young Joo, Yoon, Moon-Young +2 more·2016·NeuroToxicology

Abstract

Oxidative stress is a well-known pathogenic mechanism of a diverse array of neurological diseases, and thus, numerous studies have attempted to identify antioxidants that prevent neuronal cell death. GV1001 is a 16-amino-acid peptide derived from human telomerase reverse transcriptase (hTERT). Considering that hTERT has a strong antioxidant effect, whether GV1001 also has an antioxidant effect is a question of interest. In the present study, we aimed to investigate the effects of GV1001 against oxidative stress in neural stem cells (NSCs). Primary culture NSCs were treated with different concentrations of GV1001 and/or hydrogen peroxide (H2O2) for various time durations. The H2O2 decreased the viability of the NSCs in a concentration-dependent manner, with 200μM H2O2 significantly decreasing both proliferation and migration. However, treatment with GV1001 rescued the viability, proliferation and migration of H2O2-injured NSCs. Consistently, free radical levels were increased in rat NSCs treated with H2O2, while co-treatment with GV1001 significantly reduced these levels, especially the intracellular levels. In addition, GV1001 restored the expression of survival-related proteins and reduced the expression of death-associated ones in NSCs treated with H2O2. In conclusion, GV1001 has antioxidant and neuroprotective effects in NSCs following treatment with H2O2, which appear to be mediated by scavenging free radicals, increasing survival signals and decreasing death signals.

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Crossref · 10.1016/j.neuro.2016.05.022

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  • In rat neuronal stem cells, GV1001 blocked Aβ oligomer-induced toxicity and increased the survival of neuronal cells exposed to oxidative stress.

    “In rat neuronal stem cells, GV1001 blocked Aβ oligomer-induced toxicity and increased the survival of neuronal cells exposed to oxidative stress [91,92].”

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Authors
Park, H.-H., Yu, H.-J., Kim, S., Kim, G., Choi, N.-Y., Lee, E.-H., Lee, Y. J., Yoon, M.-Y., Lee, K.-Y., & Koh, S.-H.
Affiliations
  • Hanyang University (KR)
  • Bundang Jesaeng Hospital (KR)
  • GemVax & KAEL (South Korea) (KR)
Corresponding author
  • Lee, Kyu-Yong
  • Koh, Seong-Ho
Venue
NeuroToxicology
Publisher
Elsevier BV
Published
2016-07
Volume
55
Pages
131-141
ISSN
0161-813X (ISSN-L)
OpenAlex
W2413937595
Cited by
49
References
35
Citations by year
2026: 5 · 2025: 5 · 2024: 5 · 2023: 10 · 2022: 2 · 2021: 6 · 2020: 3 · 2019: 2 · 2018: 7 · 2017: 4
FWCI
2.25
Type
journal article
Language
en
Open access
closed
Locations
  • NeuroToxicology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Korea Science and Engineering Foundation
  • Ministry of Education, Science and Technology (2007-04717)
  • Ministry of Science, ICT and Future Planning (2015R1A2A2A04004865, 2015R1D1A1A01060644)
  • National Research Foundation of Korea
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
GV1001, neural stem cells, oxidative stress, hydrogen peroxide, antioxidant peptides, human telomerase reverse transcriptase, free radical scavenging, neuroprotection, cell survival signaling, cell death signaling, cell proliferation and migration
MeSH terms
Animals, Brain, Bromodeoxyuridine, Cell Movement, Cell Survival, Cells, Cultured, DNA Damage, Embryo, Mammalian, Hydrogen Peroxide, L-Lactate Dehydrogenase, Malondialdehyde, Peptide Fragments, Sincalide, Stem Cells, Oxidants, Annexin A5, Oxidative Stress, Telomerase, Cell Proliferation, Rats, Neural Stem Cells

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