Effects of oxygen‐free radicals on proliferation kinetics of cultured rabbit articular chondrocytes

Vincent, F.; Brun, Hervé; Clain, Elisabeth; Ronot, Xavier; Adolphe, M

doi:10.1002/jcp.1041410205

Cited by 35 publications

(14 citation statements)

References 18 publications

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“…In this work, we have focused on regulation ofexpression oftwo ofthese genes, histone and thymidine kinase (TK), in SV4OT-T2 cells exposed to hyperoxia. These genes are of particular interest as they are induced at the GI /S boundary, and several investigators have reported that inhibition of cell proliferation by reactive°2 species is characterized by arrest of cells late in the cell cycle ( 13,14). For this study, results were compared with a similarly produced SV40T lung fibroblast (SV40T-FIB) cell line and to primary lung FIB.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of lung epithelial cell proliferation by hyperoxia. Posttranscriptional regulation of proliferation-related genes.

Clément

Edeas²,

Chadelat³

et al. 1992

J. Clin. Invest.

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The alveolar surface of the lung is a major target for oxidant injury. After injury, repair of the alveolar epithelium is dependent on the ability of epithelial type 2 (T2) cells to proliferate. The regulation of T2 cell proliferation and the effect of reactive oxygen (02) species on this lung cell proliferation have not been well defined. To investigate this process we focused on the regulation of two late cell cycle genes, histone and thymidine kinase, in T2 cells and fibroblasts exposed in vitro to varying periods of hyperoxia (95% 02). Hyperoxia for 24 to 48 h arrested cell proliferation in a SV40T-immortalized T2 cell line we have developed and in primary and SV40T-immortalized lung fibroblasts. Despite the cessation of proliferation, histone and TK mRNA continued to be expressed at high levels; mRNA half-lives were markedly prolonged but neither protein was translated. Thus proliferation arrest induced by hyperoxia was associated with posttranscriptional control of at least two late cell cycle-related genes. This form of proliferation arrest is also seen when primary and SV40T-T2 cells but not fibroblasts are serum deprived, suggesting that T2 cells in vitro may be uniquely sensitive to alterations in their redox state and that these alterations in turn affect translational control of a subset of proliferation-related genes. (J. Clin. Invest. 1992. 90:1812-1818

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Section: Introductionmentioning

confidence: 99%

Inhibition of lung epithelial cell proliferation by hyperoxia. Posttranscriptional regulation of proliferation-related genes.

Clément

Edeas²,

Chadelat³

et al. 1992

J. Clin. Invest.

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“…In a previous work, we have demonstrated modifications in the levels of several mitochondrial transcripts in rat liver carcinomas which were associated with mtDNA alterations (Corral et al, 1989a,b). Hence, a possible role of oxygen free radicals and mitochondrial damage in transformed cells cannot be excluded.In normal chondrocytes, we demonstrated that oxygen free radicals generated by the hypoxanthine-xanthine oxidase system (HX-XO) induced proliferation kinetics perturbations (Vincent et al, 1989) which are associated with a decrease of c-myc and c-Ha-ras mR-NAs levels (Vincent et al, 1991). According to these results and because energy generated by mitochondria is essential for the survival and proliferation of eukaryotic cells (Ernster and Schatz, 1981; Fillingame 19801, we compared mitochondrial RNA levels in pseudosynchronized chondrocytes and in chondrocytes submitted to increased oxygen radical concentrations.…”

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confidence: 99%

Transient mitochondrial transcript level decay in oxidative stressed chondrocytes

Vincent

Corral‐Debrinski

Adolphe

1994

Journal Cellular Physiology

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Steady-state levels of 12S rRNA and NADH dehydrogenase subunit 4 mRNA (ND4) mitochondrial transcripts were measured on rabbit articular chondrocyte in culture. In pseudosynchronized chondrocytes, changes of mitochondrial RNA levels were observed during the progression of the cells in the cell cycle. Oxidative stress generated by the hypoxanthine-xanthine oxidase system (HX-XO) induced a transient decrease in the levels of both ND4 and 12S rRNA. Mitochondrial RNA levels recovered 24 h after the oxidative stress. These RNA level changes were not associated with modifications in the structure or the copy number of the mitochondrial genome. Furthermore, the decrease in the amount of the mitochondrial transcripts observed may be related to a transient inhibition of mitochondrial transcription since the treatment of cells with ethidium bromide (a mitochondrial transcription inhibitor) resulted in the same decrease in 12S rRNA level as HX-XO treatment alone.

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“…A few reports have shown evidence indicating that different cell types exposed to hydrogen peroxide display a reduced rate of proliferation, an increased multinucleation, expanded cell size, higher protein content pointing to cellular hypertrophy, premature senescence, as well as a higher prevalence of apoptosis [37, 38, 39]. Additional studies have shown the existence of a dose-related effect.…”

Section: Discussionmentioning

confidence: 99%

High Glucose Induces a Hypertrophic, Senescent Mesothelial Cell Phenotype after Long in vivo Exposure

Gotloib

Shostak

Wajsbrot

et al. 1999

Nephron

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Previous studies, done using our mouse model for population analysis of the mesothelium, showed evidence indicating that in vivo, long-term exposure (up to 30 days) of the peritoneum to high-glucose (4.25% D-glucose) concentration dialysis solutions resulted in a hypertrophic mesothelial phenotype characterized by increased cell surface area, multinucleation, low proliferative capabilities, reduced cell viability, and enhanced enzymatic activity. These elements that define a senescent population of cells were not related to the pH of the fluid and its osmolality, or to the presence of buffer lactate. The present study was designed to explore the adverse effects of a lactate-free, filter-sterilized, high-D-glucose concentration solution (4.25%) at normal pH and prepared in Hanks’ buffered salt solution after 2 h, 15 and 30 days of once a day intraperitoneal injection. Analysis of our observations indicate that in vivo exposure of the mesothelium to a high-glucose concentration induced a decreased density of the cell population, made up by larger and multinucleated cells, the viability of which was significantly lower than that observed in intact unexposed mice. The prevalence of mitosis showed an early and short-lived acceleration (up to 3 days), followed by values near zero during the rest of the follow-up period. So far, the main effect of the high-glucose concentration appears to result not from a mechanism of cytotoxicity, but from a substantial change in the life cycle of the exposed cell population, leading to their premature senescence and death in apoptosis. We hypothesize that this outcome may well be mediated by sustained oxidative stress derived from both a reduced production of scavengers, as well as the increased generation of oxygen-reactive species.

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Effects of oxygen‐free radicals on proliferation kinetics of cultured rabbit articular chondrocytes

Cited by 35 publications

References 18 publications

Inhibition of lung epithelial cell proliferation by hyperoxia. Posttranscriptional regulation of proliferation-related genes.

Inhibition of lung epithelial cell proliferation by hyperoxia. Posttranscriptional regulation of proliferation-related genes.

Transient mitochondrial transcript level decay in oxidative stressed chondrocytes

High Glucose Induces a Hypertrophic, Senescent Mesothelial Cell Phenotype after Long in vivo Exposure

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