The Two Isomers of HDTIC Compounds from Astragali Radix Slow Down Telomere Shortening Rate via Attenuating Oxidative Stress and Increasing DNA Repair Ability in Human Fetal Lung Diploid Fibroblast Cells

SummaryFanconi anemia (FA) is a unique DNA damage repair pathway. Almost twenty-two genes have been identified which are associated with the FA pathway. Defect in any of those genes causes genomic instability, and the patients bear the mutation become susceptible to cancer. In our earlier work, we have identified that Fanconi anemia protein G (FANCG) protects the mitochondria from oxidative stress. In this report, we have identified eight patients having mutation (C.65G>C; p.Arg22Pro) in the N-terminal of FANCG. The mutant protein hFANCGR22P is able to repair the DNA and able to retain the monoubiquitination of FANCD2 in FANCGR22P/FGR22P cell. However, it lost mitochondrial localization and failed to protect mitochondria from oxidative stress. Mitochondrial instability in the FANCGR22P cell causes the transcriptional down-regulation of mitochondrial iron-sulphur cluster biogenesis protein Frataxin (FXN) and resulting iron deficiency of FA protein FANCJ, an iron-sulphur containing helicase involved in DNA repair.

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Collagen secretion mediated by NMDR activation in human fetal lung fibroblasts

Cell Biology International ◽

10.1042/cbi034s070a ◽

2010 ◽

Vol 34 (8) ◽

pp. S70-S70

Author(s):

MingJie WANG ◽

ZiQiang LUO ◽

Mei LU ◽

LiHong SHANG ◽

ShaoJie YUE

Keyword(s):

Fetal Lung ◽

Lung Fibroblasts ◽

Collagen Secretion ◽

Human Fetal Lung

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Genetic variants and cognitive functions in patients with brain tumors

Neuro-Oncology ◽

10.1093/neuonc/noz094 ◽

2019 ◽

Vol 21 (10) ◽

pp. 1297-1309 ◽

Cited By ~ 5

Author(s):

Denise D Correa ◽

Jaya Satagopan ◽

Axel Martin ◽

Erica Braun ◽

Maria Kryza-Lacombe ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Dna Repair ◽

Brain Tumor ◽

Brain Tumors ◽

Cell Cycle Regulation ◽

Cognitive Outcome ◽

Cholesterol Transport ◽

Tumor Patients ◽

Cycle Regulation

AbstractBackgroundPatients with brain tumors treated with radiotherapy (RT) and chemotherapy (CT) often experience cognitive dysfunction. We reported that single nucleotide polymorphisms (SNPs) in the APOE, COMT, and BDNF genes may influence cognition in brain tumor patients. In this study, we assessed whether genes associated with late-onset Alzheimer’s disease (LOAD), inflammation, cholesterol transport, dopamine and myelin regulation, and DNA repair may influence cognitive outcome in this population.MethodsOne hundred and fifty brain tumor patients treated with RT ± CT or CT alone completed a neurocognitive assessment and provided a blood sample for genotyping. We genotyped genes/SNPs in these pathways: (i) LOAD risk/inflammation/cholesterol transport, (ii) dopamine regulation, (iii) myelin regulation, (iv) DNA repair, (v) blood–brain barrier disruption, (vi) cell cycle regulation, and (vii) response to oxidative stress. White matter (WM) abnormalities were rated on brain MRIs.ResultsMultivariable linear regression analysis with Bayesian shrinkage estimation of SNP effects, adjusting for relevant demographic, disease, and treatment variables, indicated strong associations (posterior association summary [PAS] ≥ 0.95) among tests of attention, executive functions, and memory and 33 SNPs in genes involved in: LOAD/inflammation/cholesterol transport (eg, PDE7A, IL-6), dopamine regulation (eg, DRD1, COMT), myelin repair (eg, TCF4), DNA repair (eg, RAD51), cell cycle regulation (eg, SESN1), and response to oxidative stress (eg, GSTP1). The SNPs were not significantly associated with WM abnormalities.ConclusionThis novel study suggests that polymorphisms in genes involved in aging and inflammation, dopamine, myelin and cell cycle regulation, and DNA repair and response to oxidative stress may be associated with cognitive outcome in patients with brain tumors.

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Mangiferin, a naturally occurring polyphenol, mitigates oxidative stress induced premature senescence in human dermal fibroblast cells

Molecular Biology Reports ◽

10.1007/s11033-020-06074-2 ◽

2021 ◽

Author(s):

Rashi Kanoi ◽

Pooja Loachan ◽

Shubhankar Das ◽

Bola Sadashiva Satish Rao

Keyword(s):

Oxidative Stress ◽

Dermal Fibroblast ◽

Human Dermal Fibroblast ◽

Fibroblast Cells ◽

Premature Senescence ◽

Naturally Occurring ◽

Stress Induced Premature Senescence

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Caveolin-1 promotes radioresistance in rhabdomyosarcoma through increased oxidative stress protection and DNA repair

Cancer Letters ◽

10.1016/j.canlet.2021.02.005 ◽

2021 ◽

Vol 505 ◽

pp. 1-12

Author(s):

Silvia Codenotti ◽

Francesco Marampon ◽

Luca Triggiani ◽

Marco Lorenzo Bonù ◽

Stefano Maria Magrini ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Repair ◽

Caveolin 1 ◽

Stress Protection ◽

Oxidative Stress Protection

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Telomere Shortening and Psychiatric Disorders: A Systematic Review

Cells ◽

10.3390/cells10061423 ◽

2021 ◽

Vol 10 (6) ◽

pp. 1423

Author(s):

Pedro A. Pousa ◽

Raquel M. Souza ◽

Paulo Henrique M. Melo ◽

Bernardo H. M. Correa ◽

Tamires S. C. Mendonça ◽

...

Keyword(s):

Oxidative Stress ◽

Psychological Distress ◽

Mental Disorders ◽

Psychiatric Disorders ◽

Telomere Length ◽

Traumatic Stress ◽

Molecular Mechanisms ◽

Cochrane Library ◽

Telomere Shortening ◽

Anxiety Depression

Telomeres are aging biomarkers, as they shorten while cells undergo mitosis. The aim of this study was to evaluate whether psychiatric disorders marked by psychological distress lead to alterations to telomere length (TL), corroborating the hypothesis that mental disorders might have a deeper impact on our physiology and aging than it was previously thought. A systematic search of the literature using MeSH descriptors of psychological distress (“Traumatic Stress Disorder” or “Anxiety Disorder” or “depression”) and telomere length (“cellular senescence”, “oxidative stress” and “telomere”) was conducted on PubMed, Cochrane Library and ScienceDirect databases. A total of 56 studies (113,699 patients) measured the TL from individuals diagnosed with anxiety, depression and posttraumatic disorders and compared them with those from healthy subjects. Overall, TL negatively associates with distress-related mental disorders. The possible underlying molecular mechanisms that underly psychiatric diseases to telomere shortening include oxidative stress, inflammation and mitochondrial dysfunction linking. It is still unclear whether psychological distress is either a cause or a consequence of telomere shortening.

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NME3 Regulates Mitochondria to Reduce ROS-Mediated Genome Instability

International Journal of Molecular Sciences ◽

10.3390/ijms21145048 ◽

2020 ◽

Vol 21 (14) ◽

pp. 5048

Author(s):

Chih-Wei Chen ◽

Ning Tsao ◽

Wei Zhang ◽

Zee-Fen Chang

Keyword(s):

Oxidative Stress ◽

Dna Repair ◽

Genome Stability ◽

Nuclear Dna ◽

Genome Instability ◽

Mitochondrial Fission ◽

Nucleoside Diphosphate Kinase ◽

Mitochondrial Fusion ◽

Mitochondrial Outer Membrane ◽

Mitochondrial Oxidative Stress

NME3 is a member of the nucleoside diphosphate kinase (NDPK) family that binds to the mitochondrial outer membrane to stimulate mitochondrial fusion. In this study, we showed that NME3 knockdown delayed DNA repair without reducing the cellular levels of nucleotide triphosphates. Further analyses revealed that NME3 knockdown increased fragmentation of mitochondria, which in turn led to mitochondrial oxidative stress-mediated DNA single-strand breaks (SSBs) in nuclear DNA. Re-expression of wild-type NME3 or inhibition of mitochondrial fission markedly reduced SSBs and facilitated DNA repair in NME3 knockdown cells, while expression of N-terminal deleted mutant defective in mitochondrial binding had no rescue effect. We further showed that disruption of mitochondrial fusion by knockdown of NME4 or MFN1 also caused mitochondrial oxidative stress-mediated genome instability. In conclusion, the contribution of NME3 to redox-regulated genome stability lies in its function in mitochondrial fusion.

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