scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

The Impact of 5-Azacytidine on Placental Weight, Glycoprotein Pattern and Proliferating Cell Nuclear Antigen Expression in Rat Placenta

Placenta ◽  
2007 ◽  
Vol 28 (8-9) ◽  
pp. 803-811 ◽  
Author(s):  
L. Šerman ◽  
M. Vlahović ◽  
M. Šijan ◽  
F. Bulić-Jakuš ◽  
A. Šerman ◽  
...  
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Placental Weight ◽  
Nuclear Antigen ◽  
The Impact ◽  
Proliferating Cell

Involvement of proliferating cell nuclear antigen (cyclin) in DNA replication in living cells

1989 ◽  
Vol 9 (1) ◽  
pp. 57-66
Author(s):  
M Zuber ◽  
E M Tan ◽  
M Ryoji
Keyword(s):  
Dna Polymerase ◽  
Proliferating Cell Nuclear Antigen ◽  
Living Cells ◽  
Nuclear Antigen ◽  
Plasmid Replication ◽  
Dna Polymerase Delta ◽  
Dna Polymerase Alpha ◽  
Proliferating Cell

Proliferating cell nuclear antigen (PCNA) (also called cyclin) is known to stimulate the activity of DNA polymerase delta but not the other DNA polymerases in vitro. We injected a human autoimmune antibody against PCNA into unfertilized eggs of Xenopus laevis and examined the effects of this antibody on the replication of injected plasmid DNA as well as egg chromosomes. The anti-PCNA antibody inhibited plasmid replication by up to 67%, demonstrating that PCNA is involved in plasmid replication in living cells. This result further implies that DNA polymerase delta is necessary for plasmid replication in vivo. Anti-PCNA antibody alone did not block plasmid replication completely, but the residual replication was abolished by coinjection of a monoclonal antibody against DNA polymerase alpha. Anti-DNA polymerase alpha alone inhibited plasmid replication by 63%. Thus, DNA polymerase alpha is also required for plasmid replication in this system. In similar studies on the replication of egg chromosomes, the inhibition by anti-PCNA antibody was only 30%, while anti-DNA polymerase alpha antibody blocked 73% of replication. We concluded that the replication machineries of chromosomes and plasmid differ in their relative content of DNA polymerase delta. In addition, we obtained evidence through the use of phenylbutyl deoxyguanosine, an inhibitor of DNA polymerase alpha, that the structure of DNA polymerase alpha holoenzyme for chromosome replication is significantly different from that for plasmid replication.

Ki-S1 and Proliferating Cell Nuclear Antigen Expression of Bone Marrow Macrophages

1994 ◽  
Vol 91 (3) ◽  
pp. 144-149 ◽  
Author(s):  
B.R. Titius ◽  
J. Thiele ◽  
H. Schaefer ◽  
H. Kreipe ◽  
R. Fischer
Keyword(s):  
Bone Marrow ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Proliferating Cell

Proliferating cell nuclear antigen expression on tongue of mice after intake of, or topical exposure to, alcohol

Alcohol ◽  
2003 ◽  
Vol 31 (1-2) ◽  
pp. 25-30 ◽  
Author(s):  
Fábio L.D.M. Maito ◽  
Pantelis V. Rados ◽  
Manoel Sant'Ana Filho ◽  
João J. Barbachan ◽  
Onofre Quadros
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Proliferating Cell

Proliferating cell nuclear antigen expression is increased in small bowel epithelium in the elderly

1998 ◽  
Vol 104 (1) ◽  
pp. 1-9 ◽  
Author(s):  
G.R Corazza ◽  
L Ginaldi ◽  
G Quaglione ◽  
F Ponzielli ◽  
L Vecchio ◽  
...  
Keyword(s):  
Small Bowel ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
The Elderly ◽  
Nuclear Antigen ◽  
Proliferating Cell

scholarly journals TRIM28 functions as the SUMO E3 ligase for PCNA in prevention of transcription induced DNA breaks

2020 ◽  
Vol 117 (38) ◽  
pp. 23588-23596
Author(s):  
Min Li ◽  
Xiaohua Xu ◽  
Chou-Wei Chang ◽  
Yilun Liu
Keyword(s):  
Rna Polymerase Ii ◽  
Proliferating Cell Nuclear Antigen ◽  
E3 Ligase ◽  
Nuclear Antigen ◽  
Dna Breaks ◽  
Interacting Protein ◽  
Proteomic Approach ◽  
Sumo E3 Ligase ◽  
Proliferating Cell

In human cells, the DNA replication factor proliferating cell nuclear antigen (PCNA) can be conjugated to either the small ubiquitinlike modifier SUMO1 or SUMO2, but only SUMO2-conjugated PCNA is induced by transcription to facilitate resolution of transcription–replication conflict (TRC). To date, the SUMO E3 ligase that provides substrate specificity for SUMO2-PCNA conjugation in response to TRC remains unknown. Using a proteomic approach, we identified TRIM28 as the E3 ligase that catalyzes SUMO2-PCNA conjugation. In vitro, TRIM28, together with the RNA polymerase II (RNAPII)-interacting protein RECQ5, promotes SUMO2-PCNA conjugation but inhibits SUMO1-PCNA formation. This activity requires a PCNA-interacting protein (PIP) motif located within the bromodomain of TRIM28. In cells, TRIM28 interaction with PCNA on human chromatin is dependent on both transcription and RECQ5, and SUMO2-PCNA level correlates with TRIM28 expression. As a consequence, TRIM28 depletion led to RNAPII accumulation at TRC sites, and expression of a TRIM28 PIP mutant failed to suppress TRC-induced DNA breaks.

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