Altered expression of base excision repair genes in response to high glucose-induced oxidative stress in HepG2 hepatocytes
Open accessAbstract
BACKGROUND: It is widely accepted that chronic hyperglycemia induces DNA oxidative damage in type 2 diabetes, but little is known about the effect of hyperglycemia on the DNA repair system which plays a critical role in the maintenance of genomic DNA stability in diabetes. MATERIAL/METHODS: To investigate the alteration of base excision repair (BER) genes under hyperglycemia, the relative expression of the mRNAs of the BER genes--ogg1, polbeta, lig3, xrcc1, and parp1--were quantified using real-time PCR in HepG2 hepatocytes incubated with 5.5 mM or 30 mM glucose. RESULTS: High levels of glucose induced ROS accumulation and DNA damage, paralleling the dynamic alterations of BER mRNA expression. Compared to 5.5 mM glucose-treated cells, ogg1 and polbeta mRNA expression transiently increased at day 1 and decreased after day 4 in cells exposed to 30 mM glucose. Exposure to 30 mM glucose increased the activity of PARP1, which led to reduced cellular NAD content and insulin receptor phosphorylation. CONCLUSIONS: Exposure to high concentrations of glucose initially led to the increased expression of BER mRNAs to counteract hyperglycemia-induced DNA damage; however, long-term exposure to high glucose concentrations reduced the expression of mRNA from BER genes, leading to accumulated DNA damage.
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In a study on hyperglycemia, exposure to high levels of glucose resulted in increased levels of ROS in hepatocytes; initially this led to increased expression of DNA repair genes, but long-term exposure eventually led to reduced expression of DNA repair genes and subsequent accumulation of DNA damage.
“In a study on hyperglycemia, for example, it was found that exposure to high levels of glucose resulted in increased levels of ROS in hepatocytes [122]. Initially, this led to increased expression of DNA repair genes, however long-term exposure eventually led to the reduced expression of DNA repair genes and subsequent accumulation of DNA damage [122].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [122]
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DNA repair deficiency and senescence in concussed professional athletes involved in contact sports
Schwab, N., Grenier, K., & Hazrati, L.-N. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0822-3 · Cited by 47 · see citing works
- Authors
- Pang, J., Xi, C., Dai, Y., Gong, H., & Zhang, T.-M.
- Affiliations
- Beijing Hospital (CN)
- Beijing Normal University (CN)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Ministry of Health, China
- Venue
- Medical Science Monitor
- Published
- 2012
- Volume
- 18
- Issue
- 7
- Pages
- BR281-BR285
- ISSN
- 1234-1010 (ISSN-L)
- PMC
- PMC3560773
- OpenAlex
- W2068087876
- Cited by
- 26
- References
- 21
- Citations by year
- 2024: 2 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 5 · 2016: 3 · 2015: 4 · 2014: 1 · 2012: 1
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Medical Science Monitor (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- base excision repair, hyperglycemia, oxidative stress, DNA damage, type 2 diabetes, HepG2 cells, OGG1, PARP1, NAD+ depletion, insulin receptor phosphorylation, reactive oxygen species, DNA repair gene expression
- MeSH terms
- DNA Damage, DNA Repair, Enzyme Activation, Glucose, Humans, Insulin, NAD, Phosphorylation, Poly(ADP-ribose) Polymerases, Receptor, Insulin, RNA, Messenger, Transcription, Genetic, Gene Expression Regulation, Neoplastic, Reactive Oxygen Species, Oxidative Stress, Hepatocytes, Hep G2 Cells
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