Senescence-associated cell death of human endothelial cells: the role of oxidative stress

Unterluggauer, Hermann

doi:10.1016/j.exger.2003.08.007

Cited by 112 publications

(90 citation statements)

References 56 publications

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“…The relationship between ageing and oxidative stress was verified in SCD, SCG and CR by evaluating the amount of ROS production with Dihydrorhodamine 123 (DHR123) [30,31]. A relatively low and comparable ROS production was observed in yeast cells in the exponential growth phase independent of the different carbon sources (data not shown).…”

Section: Resultsmentioning

confidence: 95%

Different carbon sources affect lifespan and protein redox state during Saccharomyces cerevisiae chronological ageing

Magherini

Carpentieri

Amoresano

et al. 2009

Cell. Mol. Life Sci.

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Abstract. In this study, a proteomic approach that combines selective labelling of proteins containing reduced cysteine residues with two-dimensional electrophoresis/mass spectrometry was used to evaluate the redox state of protein cysteines during chronological ageing in Saccharomyces cerevisiae. The procedure was developed on the grounds that biotinconjugated iodoacetamide (BIAM) specifically reacts with reduced cysteine residues. BIAM-labelled proteins can then be selectively isolated by streptavidin affinity capture. We compared cells grown on 2 % glucose in the exponential phase and during chronological ageing and we found that many proteins undergo cysteine oxidation. The target proteins include enzymes involved in glucose metabolism. Both caloric restriction and growth on glycerol resulted in a decrease in the oxidative modification. Furthermore, in these conditions a reduced production of ROS and a more negative glutathione half cell redox potential were observed.

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Section: Resultsmentioning

confidence: 95%

Different carbon sources affect lifespan and protein redox state during Saccharomyces cerevisiae chronological ageing

Magherini

Carpentieri

Amoresano

et al. 2009

Cell. Mol. Life Sci.

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“…Oxidative stress has been found to induce cell senescence in vitro and there is in vivo evidence for agerelated oxidative stress in many tissues [13][14][15]. As additional evidence for a role of ROS in aging, increased expression of the antioxidant enzyme catalase in mitochondria of transgenic mice can extend life-span and reduce age-related changes in tissues such as that of the heart [10][11][12]. It is well known that damaged mitochondria release harmful ROS into the cytosol [25][26][27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

“…Senescence may have evolved as a mechanism to prevent cells with damaged DNA from being replicated and thus to prevent tumour formation [31,32]. Replicative senescence is associated with changes in DNA structure and function including a telomere shortening and decrease activity of telomerase [10][11][12]. However, senescence appears to be much more complex than as a simple cell-cycle arrest occurring after a finite number of cell divisions.…”

Section: Discussionmentioning

confidence: 99%

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Accelerated premature stress-induced senescence of young annulus fibrosus cells of rats by high glucose-induced oxidative stress

Park

et al. 2014

International Orthopaedics (SICOT)

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Purposes Diabetes mellitus (DM) is thought to be an important aetiological factor in intervertebral disc degeneration. A glucose-mediated increase of oxidative stress is a major causative factor in development of diseases associated with DM. The aim of this study was to investigate the effect of high glucose on mitochondrial damage, oxidative stress and senescence of young annulus fibrosus (AF) cells. Methods AF cells were isolated from four-week-old young rats, cultured, and placed in either 10 % FBS (normal control) or 10 % FBS plus two different high glucose concentrations (0.1 M and 0.2 M) (experimental conditions) for one and three days. We identified and quantified the mitochondrial damage and reactive oxygen species (ROS) (oxidative stress). We also identified and quantified the occurrence of senescence and telomerase activity. Finally, the expressions of proteins were determined related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB). Results Two high glucoses enhanced the mitochondrial damage in young rat AF cells, which resulted in an excessive generation of ROS in a dose-and time-dependent manner for one and three days compared to normal control. Two high glucose concentrations increased the occurrence of senescence of young AF cells in a dose-and time-dependent manner. Telomerase activity declined in a dose-and timedependent manner. Both high glucose treatments increased the expressions of p16 and pRB proteins in young rat AF cells for one and three days. However, compared to normal control, the expressions of p53 and p21 proteins were decreased in young rat AF cells treated with both high glucoses for one and three days. Conclusions The present study demonstrated that high glucose-induced oxidative stress accelerates premature stress-induced senescence in young rat AF cells in a doseand time-dependent manner rather than replicative senescence. These results suggest that prevention of excessive generation of oxidative stress by strict blood glucose control could be important to prevent or to delay premature intervertebral disc degeneration in young patients with DM.

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“…An increase in oxidative stress and ROS production has been reported to occur with cellular senescence in several human cell types, including both human fibroblasts (Goldstein and Korczack 1981;Martinez et al 1987) and endothelial cells (Ungvari et al 2008;Unterluggauer et al 2003Unterluggauer et al , 2007. It was shown that the proportion of damaged proteins increases with replicative senescence in several cell types, including human diploid fibroblasts (HDF) (Ahmed et al 2007;Grune et al 2001;Petropoulos et al 2000) and human umbilical vein endothelial cells (HUVEC) (Unterluggauer et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Identification of Hsc70 as target for AGE modification in senescent human fibroblasts

et al. 2008

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Cellular senescence is known as a potent mechanism of tumor suppression, and cellular senescence in vitro also reflects at least some features of aging in vivo. The Free Radical Theory of aging suggests that reactive oxygen species are important causative agents of aging and cellular senescence. Besides damage of nucleic acids and lipids, also oxidative modifications of proteins have been described as potential causative events in the senescence response. However, the identity of protein targets for post-translational modifications in senescent cells has remained unclear. In the present communication, we analyzed the occurrence of oxidative posttranslational modifications in senescent human endothelial cells and dermal fibroblasts. We found a significant increase in the level of protein carbonyls and AGE modification with senescence in both cell types. Using 2D-Gel electrophoresis and Western Blot we found that heat shock cognate protein 70 is a bona fide target for AGE modification in human fibroblasts.

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Senescence-associated cell death of human endothelial cells: the role of oxidative stress

Cited by 112 publications

References 56 publications

Different carbon sources affect lifespan and protein redox state during Saccharomyces cerevisiae chronological ageing

Different carbon sources affect lifespan and protein redox state during Saccharomyces cerevisiae chronological ageing

Accelerated premature stress-induced senescence of young annulus fibrosus cells of rats by high glucose-induced oxidative stress

Identification of Hsc70 as target for AGE modification in senescent human fibroblasts

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