Uptake of Foreign Nucleic Acids in Kidney Tubular Epithelial Cells Deficient in Proapoptotic Endonucleases

Buzder, Timea; Yin, Xiaoyan; Wang, Xiaoying; Bánfalvi, Gáspár; Basnakian, Alexei G.

doi:10.1089/dna.2008.0850

Cited by 16 publications

(10 citation statements)

References 34 publications

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“…Digital images of the gel were acquired using FluorChem HD2 system (ProteinSimple, Santa Clara, CA) with UV light. The relative amount of endonuclease activity was calculated based on the density of the three bands for plasmid DNA present in covalently closed circular DNA (Type I), open circular DNA (Type I), or linear DNA (Type III) as was previously described 20, 21 .…”

Section: Methodsmentioning

confidence: 99%

Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice

Albadawi

Öklü

Malley

et al. 2016

Journal of Vascular Surgery

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Objective Extracellular traps-(ETs) consist of DNA-protein-complexes formed following tissue injury contributes to the inflammatory and thrombosis cascades thereby exacerbating injury. Exogenous DNase-1 has been suggested as a therapeutic strategy to limit injury in the brain and myocardium.. These studies were designed to evaluate the effects of exogenous DNase-I treatment on skeletal muscle injury following acute hind limb ischemia-reperfusion (IR) injury in mice, and to determine whether neutrophils were a major source of ETs in postischemic muscle tissue. Methods C57BL6 mice were subjected to 1.5 hrs tourniquet ischemia and 24 hrs reperfusion with and without human recombinant DNase-I treatment. A separate set of mice was subjected to neutrophil depletion, followed by the same intervals of IR. Laser Doppler imaging and tissue harvesting was done at 24 hrs for assessment of limb perfusion, muscle fiber injury, ATP, markers of inflammation, thrombosis, and ETs formation. Results DNase-I treatment significantly reduced ETs detection in post-ischemic muscle but did not alter skeletal muscle fiber injury, levels of pro-inflammatory molecules or ATP. DNase-I treatment did enhance postischemic hind limb perfusion, decreased infiltrating inflammatory cells and reduced the expression of Thrombin-Anti-Thrombin-III. Neutrophil depletion resulted in a significant yet small reduction in ETs in the post ischemic muscle. Neutrophil depletion did not alter skeletal muscle fiber injury, hind limb perfusion, or ATP levels. Conclusions These data suggest that neither DNase-I treatment nor Neutrophil depletion were protective against IR injury, even though both decreased ETs detection in skeletal muscle following IR. Neutrophils are not the only source of ETs following IR.

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Section: Methodsmentioning

confidence: 99%

Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice

Albadawi

Öklü

Malley

et al. 2016

Journal of Vascular Surgery

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“…However, 99% of the time DNA fragmentation is provided by endogenous cellular enzymes traditionally called "apoptotic endonucleases" (Hengartner, 2001). Studies showed that same enzymes participate in other types of cell death, particularly, necrosis (Singh et al, 2013), and prevent the entering of extracellular DNA into the cell (Buzder et al, 2009). Most studied of these endonucleases are deoxyribonuclease I (DNase I) and endonuclease G (EndoG).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of graphene‐induced cytotoxicity: Role of endonucleases

Fahmi

Branch

Nima

et al. 2017

J of Applied Toxicology

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Graphene, a crystalline allotrope or carbon, presents numerous useful properties; however, its toxicity is yet to be determined. One of the most dramatic and irreversible toxic abilities of carbon nanomaterials is the induction of DNA fragmentation produced by endogenous cellular endonucleases. This study demonstrated that pristine graphene exposed to cultured kidney tubular epithelial cells is capable of inducing DNA fragmentation measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, which is usually associated with cell death. TUNEL (cell death) and endonuclease activity measured using a near infrared fluorescence probe was significantly higher in cells containing graphene aggregates detected by Raman spectroscopy. The elevation of TUNEL coincided with the increased abundance of heme oxygenase 1 (HO-1), heat shock protein 90 (HSP90), active caspase-3 and endonucleases (deoxyribonuclease I [DNase I] and endonuclease G [EndoG]), as measured by quantitative immunocytochemistry. Specific inhibitors for HO-1, HSP90, caspase-3, DNase I and EndoG almost completely blocked the DNA fragmentation induced by graphene exposure. Therefore, graphene induces cell death through oxidative injury, caspase-mediated and caspase-independent pathways; and endonucleases DNase I and EndoG are important for graphene toxicity. Inhibition of these pathways may ameliorate cell injury produced by graphene.

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“…DNase I is mainly expressed in tubular epithelial cells, where it represent 80% of all endonuclease activity [ 33 , 46 ]. However, DNase I is also found in glomeruli [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease

et al. 2017

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FcγRIIB-/-yaa mice develop severe lupus glomerulonephritis due to lack of an inhibitory immune cell receptor combined with a Y-chromosome linked autoimmune accelerator mutation. In the present study, we have investigated nephritis development and progression in FcγRIIB-/-yaa mice to find shared features with NZB/NZW F1 lupus prone mice and human disease. We sacrificed 25 male FcγRIIB-/-yaa mice at various disease stages, and grouped them according to activity and chronicity indices for lupus nephritis. Glomerular morphology and localization of electron dense deposits containing IgG were further determined by immune electron microscopy. Renal DNase I and pro-inflammatory cytokine mRNA levels were measured by real-time quantitative PCR. DNase I protein levels was assessed by immunohistochemistry and zymography. Our results demonstrate early development of electron dense deposits containing IgG in FcγRIIB-/-yaa mice, before detectable levels of serum anti-dsDNA antibodies. Similar to NZB/NZW F1, electron dense deposits in FcγRIIB-/-yaa progressed from being confined to the mesangium in the early stage of lupus nephritis to be present also in capillary glomerular basement membranes. In the advanced stage of lupus nephritis, renal DNase I was lost on both transcriptional and protein levels, which has previously been shown in NZB/NZW F1 mice and in human disease. Although lupus nephritis appears on different genetic backgrounds, our findings suggest similar processes when comparing different murine models and human lupus nephritis.

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Uptake of Foreign Nucleic Acids in Kidney Tubular Epithelial Cells Deficient in Proapoptotic Endonucleases

Cited by 16 publications

References 34 publications

Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice

Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice

Mechanism of graphene‐induced cytotoxicity: Role of endonucleases

Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease

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