Cisplatin Nephrotoxicity Is Mediated by Deoxyribonuclease I

Basnakian, Alexei G.; Apostolov, Eugene O.; Yin, Xiaoyan; Napirei, Markus; Mannherz, Hans Georg; Shah, Sudhir V.

doi:10.1681/asn.2004060494

Cited by 108 publications

(106 citation statements)

References 39 publications

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“…DNA was extracted from cultured NRK-52E cells using DNeasy blood and tissue kit (Qiagen). DNA or RNA electrophoresis in agarose gel was performed as described previously (Basnakian et al, 2005).…”

Section: Rna and Dna Extractionmentioning

confidence: 99%

“…However, in response to stress, endonucleases become activated and are released from cellular compartments to reach nuclear DNA, thus completely destroying it within a few hours after cell injury or cell death. Therefore, inactivation of endonucleases before cell/tissue injury is usually cytoprotective (Basnakian et al, 2005;Napirei et al, 2006;Apostolov et al, 2007Apostolov et al, , 2009Apostolov et al, , 2011.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of Apoptotic Endonucleases by EndoG

Zhdanov

Fahmi

Wang

et al. 2015

DNA and Cell Biology

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Cells contain several apoptotic endonucleases, which appear to act simultaneously before and after cell death by destroying the host cell DNA. It is largely unknown how the endonucleases are being induced and whether they can regulate each other. This study was performed to determine whether apoptotic mitochondrial endonuclease G (EndoG) can regulate expression of other apoptotic endonucleases. The study showed that overexpression of mature EndoG in kidney tubular epithelial NRK-52E cells can increase expression of caspase-activated DNase (CAD) and four endonucleases that belong to DNase I group including DNase I, DNase X, DNase IL2, and DNase g, but not endonucleases of the DNase 2 group. The induction of DNase I-type endonucleases was associated with DNA degradation in promoter/exon 1 regions of the endonuclease genes. These results together with findings on colocalization of immunostained endonucleases and TUNEL suggest that DNA fragmentation after EndoG overexpression was caused by DNase I endonucleases and CAD in addition to EndoG itself. Overall, these data provide first evidence for the existence of the integral network of apoptotic endonucleases regulated by EndoG.

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Section: Rna and Dna Extractionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Regulation of Apoptotic Endonucleases by EndoG

Zhdanov

Fahmi

Wang

et al. 2015

DNA and Cell Biology

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“…2B). As shown by our previous studies, specific activity of DNase I in cultured cells is much lower that in tissues [27]. To produce in vivo breast cancer tumors, MCF-7 and ZR-75-1 cells, as well as another tumorigenic human breast cancer cells, BT-474, were injected in nude mice and xenografts were grown as it was described in Materials and Methods.…”

Section: Endonucleases In Breast Cancer Cell Linesmentioning

confidence: 99%

Endonuclease G promotes cell death of non-invasive human breast cancer cells

Basnakian

Apostolov

Yin

et al. 2006

Experimental Cell Research

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The invasiveness of breast cancer cells was shown to be associated with the suppressed ability to develop apoptosis. The role of cell death DNases/endonucleases has not been previously examined in relation with the invasiveness of breast cancer cells. We have compared the activity of the endonucleases in seven human breast cancer cell lines different in the level of invasiveness and differentiation. The invasiveness of cell lines was confirmed by an in vitro Matrigel-based assay. The total endonuclease activity in the differentiated non-invasive (WDNI) cell lines was higher than that in the poorly differentiated invasive (PDI) cells. The expression of EndoG strongly correlated with the degree of estrogen receptor expression and showed an inverse correlation with vimentin and matrix metalloproteinase-13. The EndoG-positive WDNI cells were more sensitive to etoposide-or camptothecin-induced cell death than EndoG-negative PDI cells. Silencing of EndoG caused inhibited of SK-BR-3 WDNI cell death induced by etoposide. Human ductal carcinomas in situ expressed high levels of EndoG, while invasive medullar and ductal carcinomas had significantly decreased expression of EndoG. This correlated with decreased apoptosis as measured by TUNEL assay. Our findings suggest that the presence of EndoG in non-invasive breast cancer cells determines their sensitivity to apoptosis, which may be taken into consideration for developing the chemotherapeutic strategy for cancer treatment.

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“…Endonuclease activity in total protein extracts from kidney cells and in culture medium was determined using the plasmid incision assay (PIA) with pBR322 plasmid (New England Biolabs, Beverly, MA) as the substrate as described previously (Basnakian et al, 2005).…”

Section: Plasmid Incision Assaymentioning

confidence: 99%

“…These were the most active endonucleases in kidney tubular epithelial cells (Peitsch et al, 1995;Basnakian et al, 2005;Irvine et al, 2005). DNase I is a 31 kDa cytoplasmic enzyme that digests single-and doublestranded DNA.…”

Section: Introductionmentioning

confidence: 99%

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

Buzder

Yin

Wang

et al. 2009

DNA and Cell Biology

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Degradation of DNA during gene delivery is an obstacle for gene transfer and for gene therapy. DNases play a major role in degrading foreign DNA. However, which of the DNases are involved and whether their inactivation can improve gene delivery have not been studied. We have recently identified deoxyribonuclease I (DNase I) and endonuclease G (EndoG) as the major degradative enzymes in the mouse kidney proximal tubule epithelial (TKPTS) cells. In this study, we used immortalized mouse TKPTS cells and primary tubular epithelial cells isolated from DNase I or EndoG knockout (KO) mice and examined the degradation of plasmid DNA during its uptake. DNase I and EndoG KO cells showed a higher rate of transfection by pECFP-N1 plasmid than wild-type cells. In addition, EndoG KO cells prevented the uptake of fluorescent-labeled RNA. Complete inhibition of secreted DNase I by G-actin did not improve plasmid transfection, indicating that only intracellular DNase I affects DNA stability. Data demonstrate the importance of DNase I and EndoG in host cell defense against gene and RNA delivery to renal tubular epithelial cells in vitro.

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Cisplatin Nephrotoxicity Is Mediated by Deoxyribonuclease I

Cited by 108 publications

References 39 publications

Regulation of Apoptotic Endonucleases by EndoG

Regulation of Apoptotic Endonucleases by EndoG

Endonuclease G promotes cell death of non-invasive human breast cancer cells

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

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