Evaluating Gamma-H2AX Expression as a Biomarker of DNA Damage after X-ray in Angiography Patients

Alipoor, Alieh; Fardid, Reza; Sharifzadeh, Sedigheh

doi:10.31661/jbpe.v8i4dec.768

Cited by 10 publications

(10 citation statements)

References 26 publications

(39 reference statements)

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“…Among the three biomarkers used, the γ-H2AX foci assay, demonstrated a positive correlation between the frequency of γ-H2AX foci and the fluoroscopy time (r = 0.520 and p = 0.013) and a linear positive correlation between the frequency of γ-H2AX foci and effective dose (r = 0.540 and p = 0.010). This result is in accordance with earlier studies that reported a positive correlation in patients exposed to low radiation doses (35,36).…”

Section: Discussionsupporting

confidence: 94%

“…At a molecular level, there are certain studies that report an increase of DSBs after exposure to low ionizing radiation doses. Kuefner et al (34) and Alipoor et al (35) observed an increase in the percentage of DSBs after exposure to angiography, compared to pre-exposure time. Similarly, in our study, not only a statistically significant increase in the mean value of DNA DSBs was observed for the total study group, but also at the individual level, this increase was statistically significant in the 91% of patients after their cardiac interventional procedures and residual γ-H2AX foci were still detectable in irradiated lymphocytes, 24 h after.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

The Use of Genotoxicity Endpoints as Biomarkers of Low Dose Radiation Exposure in Interventional Cardiology

Habibi

Karyofyllis

Nikolakopoulou

et al. 2021

Front. Public Health

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The effect of the reportedly low ionizing radiation doses, such as those very often delivered to patients in interventional cardiology, remains ambiguous. As interventional cardiac procedures may have a significant impact on total collective effective dose, there are radiation protection concerns for patients and physicians regarding potential late health effects. Given that very low doses (<100 mSv) are expected to be delivered during these procedures, the purpose of this study was to assess the potency and suitability of current genotoxicity biomarkers to detect and quantitate biological effects essential for risk estimation in interventional cardiology. Specifically, the biomarkers γ-H2AX foci, dicentric chromosomes, and micronuclei, which underpin radiation-induced DNA damage, were studied in blood lymphocytes of 25 adult patients before and after interventional cardiac procedures. Even though the mean values of all patients as a group for all three endpoints tested show increased yields relative to baseline following medical exposure, our results demonstrate that only the γ-H2AX biomarker enables detection of statistically significant differences at the individual level (p < 0.001) for almost all patients (91%). Furthermore, 24 h after exposure, residual γ-H2AX foci were still detectable in irradiated lymphocytes. Their decline was found to vary significantly among the individuals and the repair kinetics of γ-H2AX foci was found to range from 25 to 95.6% of their maximum values obtained.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 97%

The Use of Genotoxicity Endpoints as Biomarkers of Low Dose Radiation Exposure in Interventional Cardiology

Habibi

Karyofyllis

Nikolakopoulou

et al. 2021

Front. Public Health

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“…ATR activation facilitates chemotherapy resistance to cisplatin, 16,26,27 and ATR inhibition enhances cisplatin chemosensitivity. 9,28,29 In this study, we found that blocking ATR with the inhibitor VE-822 or with ATR shRNA upregulated the phosphorylation of H2AX, a biomarker of DNA damage, 30,31 indicating that ATR inhibition promoted cisplatin-induced DNA damage. As expected, ATR inhibition promoted cisplatin-induced inhibition of cell proliferation and cell death in chondrosarcoma cells, suggesting that VE-822 mediated inhibition of ATR is a valuable strategy for chemotherapy of chondrosarcoma with cisplatin.…”

Section: Discussionmentioning

confidence: 60%

<p>VE-822 mediated inhibition of ATR signaling sensitizes chondrosarcoma to cisplatin via reversion of the DNA damage response</p>

Liang¹,

Yang²,

Wang³

et al. 2019

OTT

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Introduction: Cisplatin has been reported to elicit the DNA damage response (DDR) via activation of the ATR-Chk1 pathway, which in turn contributes to the induction of cisplatin resistance. Inhibition of ATR-Chk1 signaling reverses cisplatin resistance in some cancers. However, the influence of inhibiting ATR-Chk1 signaling on cisplatin resistance in chondrosarcoma cancer has not been reported. Materials and methods: We compared the expression levels of ATR kinases in human nasopharyngeal carcinoma, choriocarcinoma and chondrosarcoma cell lines. We inhibited ATR kinase function with VE-822, a selective ATR inhibitor, and suppressed ATR kinase expression with shRNA. Western blotting, the CCK-8 assay, cell cycle distribution assay and apoptosis analysis were used to study the influence of inhibiting ATR-Chk1 signaling on reversing cisplatin resistance in chondrosarcoma cell lines. Results: We found that chondrosarcoma cells expressed very low basal levels of phosphorylated ATR, but cisplatin treatment induced the activation of ATR-Chk1 signaling in a doseand time-dependent manner, suggesting the induction of DDR. As expected, ATR inhibition with VE-822 reversed cisplatin-induced DDR and enhanced cisplatin-induced activation of H2AX, which is an important marker of DNA damage. Meanwhile, ATR inhibition by RNA interference also reversed DDR and promoted DNA damage. Furthermore, both pharmacological and molecular inhibition of ATR accelerated cisplatin-induced inhibition of cell proliferation and cell death. Conclusion: Our results suggested that inhibiting ATR activation promoted cisplatininduced cell death via reversion of DDR, and VE-822 may be a valuable strategy for the prevention of cisplatin resistance in chondrosarcoma.

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“…γ-H2AX is a DNA repair protein whose expression is commonly measured to quantify double-stranded DNA damage [ 43–45 ]. Compared with that in the control group, the expression of γ-H2AX in the 1 mM bup group was not significantly different; however, 2 mM bup increased γ-H2AX protein expression ( Figure 2 A&B).…”

Section: Resultsmentioning

confidence: 99%

P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons

et al. 2022

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The research aimed to explore the biological role of p53 protein and long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in bupivacaine (bup)-induced neurotoxicity. Our work treated dorsal root ganglion (DRG) cells with bup, detected cell viability through CCK-8, apoptosis through TUNEL assays, DeoxyriboNucleic Acid (DNA) damage through γ-H2AX protein and comet assay, including p53 mRNA, protein and TUG1 expression through q-PCR and western blot, furthermore, cell viability and DNA damage were determined after the silencing of p53 and TUG1, biological information and TUG1 FISH combined with p53 protein immunofluorescence (IF) was performed to determine the cellular localization of these molecule. In vivo experiments, we explored the impact of intrathecal injection of bup on p53 mRNA and protein, TUG1, γ-H2AX protein expression. The results showed that bup was available to signally decreased cell viability, promoted apoptosis rate and DNA damage, additionally, bup increased p53 mRNA and protein and TUG1 expression. P53 siRNA and TUG1 siRNA significantly increased DNA damage. Furthermore, bioinformatics analysis and colocalization experiments revealed that the p53 protein is a transcription factor of TUG1, in vivo experiment, intrathecal injection of bup increased the p53 mRNA, p53 protein, TUG1 and γ-H2AX protein in the murine DRG. In this study, it was found p53 and TUG1 promote the repair of the DNA damage induced by bup in murine dorsal root ganglion cells, suggesting a new strategy for the amelioration of bup-induced neurotoxicity.

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Evaluating Gamma-H2AX Expression as a Biomarker of DNA Damage after X-ray in Angiography Patients

Cited by 10 publications

References 26 publications

The Use of Genotoxicity Endpoints as Biomarkers of Low Dose Radiation Exposure in Interventional Cardiology

The Use of Genotoxicity Endpoints as Biomarkers of Low Dose Radiation Exposure in Interventional Cardiology

<p>VE-822 mediated inhibition of ATR signaling sensitizes chondrosarcoma to cisplatin via reversion of the DNA damage response</p>

P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons

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