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At least 307 records · Page 17Linked to original sources
PubMed1991

Inhibition of protein synthesis results in super-induction of procyclin (PARP) RNA levels.

Procyclin is an abundant surface antigen found exclusively on the procyclic forms of African trypanosomes. We are interested in the induction of procyclin gene expression during differentiation from bloodstream forms. We find that increased levels of procyclin RNA are evident as early as 15 min after triggering differentiation. The increase in procyclin RNA levels requires the temperature shift from 37 degrees C to 27 degrees C and is aided by addition of the tricarboxylic acid cycle intermediate cis-aconitate. Maximal induction is observed with a combination of three triggers of differentiation: citrate, cis-aconitate and the temperature shift. Protein synthesis does not appear to be required for induction of procyclin RNA during differentiation. In fact, addition of protein synthesis inhibitors results in super-induction of procyclin RNA levels, even under conditions where no induction is normally observed (i.e., at 37 degrees C in the absence of citrate and cis-aconitate). This super-induction was observed with four different protein synthesis inhibitors that affect different stages of translation. Thus, the accumulation of procyclin transcripts may be under the control of a negative regulator whose effective levels are reduced during differentiation from bloodstream to procyclic forms.

Aconitic Acid↗
PubMed2006

Mitotic phosphorylation of tankyrase, a PARP that promotes spindle assembly, by GSK3.

The assembly and function of mitotic spindles require poly(ADP-ribosyl)ation of spindle components by tankyrase, a poly(ADP-ribose) polymerase that aggregates to spindle poles during mitosis. Tankyrase itself is phosphorylated during mitosis, but the kinases involved remain undefined. Herein we report that mitotic phosphorylation of tankyrase is abrogated in cells treated with the GSK3 inhibitors LiCl and indirubin. Moreover, the electrophoretic mobility-shift of tankyrase arising from mitotic phosphorylation can be reproduced in vitro by GSK3-mediated phosphorylation. Lastly, mutagenesis study suggested that GSK3 in vitro phosphorylates tankyrase on S978, T982, S987, and S991, residues that comprise two adjacent copies of the canonical GSK3 phospho-acceptor motif [S/T]-X-X-X-[S/T]. Collectively, our data suggest that GSK3 contributes to mitotic tankyrase phosphorylation, raising the possibility that this phosphorylation might mediate some of the established roles of GSK3 in spindle assembly and mitotic progression.

3T3-L1 Cells↗
PubMed2006

Promoter cleavage: a topoIIbeta and PARP-1 collaboration.

Hormones trigger dramatic changes in the structure and transcriptional activity of specific promoters that lead to exchange of repression complexes for activation complexes. now show that estrogen-dependent restructuring and transcription of the pS2 promoter require the generation of a DNA double-strand break by a novel protein complex containing two enzymes, topoisomerase IIbeta and poly(ADP-ribose) polymerase.

DNA Topoisomerases, Type II↗
PubMed2004

Cytoprotective effects of Glycyrrhizae radix extract and its active component liquiritigenin against cadmium-induced toxicity (effects on bad translocation and cytochrome c-mediated PARP cleavage).

Glycyrrhizae radix has been popularly used as one of the oldest and most frequently employed botanicals in herbal medicine in Asian countries, and currently occupies an important place in food products. Cadmium (Cd) induces both apoptotic and non-apoptotic cell death, in which alterations in cellular sulfhydryls participate. In the present study, we determined the effects of G. radix extract (GRE) and its representative active components on cell death induced by Cd and explored the mechanistic basis of cytoprotective effects of G. radix. Incubation of H4IIE cells with GRE inhibited cell death induced by 10 microM Cd. Also, GRE effectively blocked Cd (1 microM)-induced cell death potentiated by buthionine sulfoximine (BSO) without restoration of cellular GSH. GRE prevented both apoptotic and non-apoptotic cell injury induced by Cd (10 microM) or Cd (0.3-1 microM) + BSO. Inhibition of Cd-induced cell injury by pretreatment of cells with GRE suggested that the cytoprotective effect result from alterations in the levels of the protein(s) responsible for cell viability. GRE inhibited mitochondrial Bad translocation by Cd or CD+BSO, and caused restoration of mitochondrial Bcl(xL) and cytochrome c levels. Cd-induced poly(ADP-ribose)polymerase cleavage in control cells or in cells deprived of sulfhydryls was prevented by GRE treatment. Among the major components present in GRE, liquiritigenin, but not liquiritin, isoliquiritigenin or glycyrrhizin, exerted cytoprotective effect. These results demonstrated that GRE blocked Cd-induced cell death by inhibiting the apoptotic processes involving translocation of Bad into mitochondria, decreases in mitochondrial Bcl(xL) and cytochrome c, and poly(ADP-ribose)polymerase cleavage.

Animals↗
PubMed2001

[Composite, non-resorbable parietal prosthesis with polyethylene terephtalate-polyurethane (HI-TEX PARP NT): prevention of intraperitoneal adhesions. Experimental study in rabbits].

The authors report an experimental study in the rabbit with a new composite non absorbable mesh in Polyethylene Terephtalate-Polyurethane used for incisional hernia repair in intraperitoneal positioning. This new mesh has one permeable side in polyethylene terephtalate for rapid tissue fixation and another side in polyruethane, hydrophob in order to avoid cell penetration. Eighteen rabbits were operated. A wound was created in aponeurose, muscle and peritoneal abdominal wall. The mesh was placed in intraperitoneal positioning and was taken off at 4, 9 and 13 months for histologic examination and electronic microscopical examination. Tolerance, adhesion, tissular reaction and neoperitoneum formation have been studied. All the meshes were well integrated and without sepsis. In 18% of cases small and monocclusive intraperitoneal adhesions were found. This new composite mesh in intraperitoneal positioning gave good results at medium-term in the rabbit. It's an attractive alternative for incision hernias repair with intraperitoneal mesh.

Abdominal Muscles↗
PubMed2002

GPI 6150, a PARP inhibitor, reduces the colon injury caused by dinitrobenzene sulfonic acid in the rat.

Poly (ADP-ribose) polymerase, a nuclear enzyme activated by DNA strand breaks, has been shown to play an important role in the pathogenesis of inflammatory bowel disease. Here we investigate the effects of 1,11b-dihydro-[2H]benzopyrano [4,3,2-de]isoquinolin-3-one (GPI 6150), a new poly (ADP-ribose) polymerase inhibitor, in animal models of experimental colitis. Colitis was induced in rats by intra-colonic instillation of dinitrobenzene sulfonic acid. Rats experienced hemorrhagic diarrhea and weight loss. At 4 days after administration of dinitrobenzensulfonic acid, the mucosa of the colon exhibited large areas of necrosis. Neutrophil infiltration (determined by histology and an increase in myeloperoxidase activity in the mucosa) was associated with up-regulation of ICAM-1. Immunohistochemistry for poly (ADP-ribose) showed an intense staining in the inflamed colon. GPI 6150 (20 or 40 mg/kg daily, i.p.) significantly reduced the degree of hemorrhagic diarrhea and weight loss caused by administration of dinitrobenzensulfonic acid. GPI 6150 also caused a substantial reduction of (i) the degree of colon injury, (ii) the rise in myeloperoxidase activity (mucosa), (iii) the increase in the tissue levels of malondialdehyde, (iv) the increase in staining (immunohistochemistry) for poly (ADP-ribose), as well as (v) the upregulation of ICAM-1 and P-selectin caused by dinitrobenzensulfonic acid in the colon. Thus, GPI 6150 reduces the degree of colitis caused by dinitrobenzensulfonic acid. We propose that GPI 6150 may be useful in the treatment of inflammatory bowel disease.

Animals↗
PubMed1999

2-nitroimidazol-5-ylmethyl as a potential bioreductively activated prodrug system: reductively triggered release of the PARP inhibitor 5-bromoisoquinolinone.

5-Chloromethyl-1-methyl-2-nitroimidazole reacted efficiently with the anion derived from 5-bromoisoquinolin-1-one to give 5-bromo-2-((1-methyl-2-nitroimidazol-5-yl)methyl)isoquinolin -1-one. Biomimetic reduction effected release of the 5-bromoisoquinolin-1-one. The 2-nitroimidazol-5-ylmethyl unit thus has potential for development as a general prodrug system for selective drug delivery to hypoxic tissues.

Ammonium Chloride↗