Effects of sod gene overexpression and deletion mutation on the expression profiles of reporter genes of major detoxification pathways in Caenorhabditis elegans

Back, Patricia; Matthijssens, Filip; Vlaeminck, Caroline; Braeckman, Bart P.; Vanfleteren, Jacques R.

doi:10.1016/j.exger.2010.01.014

Cited by 46 publications

(33 citation statements)

References 63 publications

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“…Thus, it was recognized that there are the time lags until the AX-dependent rising in the expression of these genes. In these genes; however, there are the genes that were regulated by other transcription factors (e.g., role of SKN-1 in ctl -genes) [27]. Therefore, the inconsistency during the intrinsic catalase activities in this paper and the mRNA levels in the previous data may depend on the diversity in transcriptional regulation of ctl genes expression [28].…”

Section: Resultsmentioning

confidence: 95%

Supplemental Cellular Protection by a Carotenoid Extends Lifespan via Ins/IGF-1 Signaling inCaenorhabditis elegans

Yazaki

Yoshikoshi

Oshiro

et al. 2011

Oxidative Medicine and Cellular Longevity

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Astaxanthin (AX), which is produced by some marine animals, is a type of carotenoid that has antioxidative properties. In this study, we initially examined the effects of AX on the aging of a model organism C. elegans that has the conserved intracellular pathways related to mammalian longevity. The continuous treatments with AX (0.1 to 1 mM) from both the prereproductive and young adult stages extended the mean lifespans by about 16–30% in the wild-type and long-lived mutant age-1 of C. elegans. In contrast, the AX-dependent lifespan extension was not observed even in a daf-16 null mutant. Especially, the expression of genes encoding superoxide dismutases and catalases increased in two weeks after hatching, and the DAF-16 protein was translocated to the nucleus in the AX-exposed wild type. These results suggest that AX protects the cell organelle mitochondria and nucleus of the nematode, resulting in a lifespan extension via an Ins/IGF-1 signaling pathway during normal aging, at least in part.

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Section: Resultsmentioning

confidence: 95%

Supplemental Cellular Protection by a Carotenoid Extends Lifespan via Ins/IGF-1 Signaling inCaenorhabditis elegans

Yazaki

Yoshikoshi

Oshiro

et al. 2011

Oxidative Medicine and Cellular Longevity

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“…Studies have identified three distinctions between regulation and function of SKN-1 in C. elegans and Nrf2 in mammals: i) DNA binding domains, ii) mechanisms of transcriptional activation, and iii) regulation of protein levels [39]. Furthermore, a cross-talk between the insulin-like pathway and the SKN-1 pathway has been reported in C. elegans (overview in [40]) which has not been reported for mammalian cells. Another relevant difference between the species might be the absence of a C. elegans homologue to human NFκB (reviewed by [41]) which is known to be inhibited by CAPE in mammalian cells [11].…”

Section: Discussionmentioning

confidence: 99%

Caffeic Acid Phenethylester Increases Stress Resistance and Enhances Lifespan in Caenorhabditis elegans by Modulation of the Insulin-Like DAF-16 Signalling Pathway

et al. 2014

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CAPE is an active constituent of propolis which is widely used in traditional medicine. This hydroxycinnamic acid derivate is a known activator of the redox-active Nrf2 signalling pathway in mammalian cells. We used C. elegans to investigate the effects of this compound on accumulation of reactive oxygen species and the modulation of the pivotal redox-active pathways SKN-1 and DAF-16 (homologues of Nrf2 and FoxO, respectively) in this model organism; these results were compared to the effects in Hct116 human colon carcinoma cells. CAPE exerts a strong antioxidative effect in C. elegans: The increase of reactive oxygen species induced by thermal stress was diminished by about 50%. CAPE caused a nuclear translocation of DAF-16, but not SKN-1. CAPE increased stress resistance of the nematode against thermal stress and finally a prolongation of the median and maximum lifespan by 9 and 17%, respectively. This increase in stress resistance and lifespan was dependent on DAF-16 as shown in experiments using a DAF-16 loss of function mutant strain. Life prolongation was retained under SKN-1 RNAi conditions showing that the effect is SKN-1 independent. The results of CAPE obtained in C. elegans differed from the results obtained in Hct116 colon carcinoma cells: CAPE also caused strong antioxidative effects in the mammalian cells, but no activation of the FoxO4 signalling pathway was detectable. Instead, an activation of the Nrf2 signalling pathway was shown by luciferase assay and western blots. CONCLUSION: CAPE activates the insulin-like DAF-16, but not the SKN-1 signalling pathway in C. elegans and therefore enhances the stress resistance and lifespan of this organism. Since modulation of the DAF-16 pathway was found to be a pivotal effect of CAPE in C. elegans, this has to be taken into account for the investigation of the molecular mechanisms of the traditional use of propolis.

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“…Thus, under basal conditions inhibitory phosphorylation by AKT-1/2 and SGK-1 (key components of the IIS pathway) inactivates SKN-1 by maintaining it in the cytosol [79]. Conversely, under conditions of oxidative stress or reduced IIS pathway activity (induced by caloric restriction), the PMK-1 protein (ortholog of the mammalian p38 MAPK) phosphorylates SKN-1 to promote its nuclear translocation and subsequently induce the transcription of phase II detoxification genes, such as gcs-1 (encoding γ -glutamyl cysteine synthetase), gst-10 (encoding isoforms of glutathione S-transferase), and sod-1 (encoding SOD) [79, 84, 85] to generate the ROS response (Figure 2). Another ROS protection mechanism is conferred by DAF-16 via the IIS pathway, which regulates MnSOD gene expression [86].…”

Section: Oxidative Stress and Diseasementioning

confidence: 99%

Caenorhabditis elegans: A Useful Model for Studying Metabolic Disorders in Which Oxidative Stress Is a Contributing Factor

Moreno-Arriola¹,

Cárdenas-Rodríguez²,

Coballase-Urrutía³

et al. 2014

Oxidative Medicine and Cellular Longevity

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Caenorhabditis elegans is a powerful model organism that is invaluable for experimental research because it can be used to recapitulate most human diseases at either the metabolic or genomic level in vivo. This organism contains many key components related to metabolic and oxidative stress networks that could conceivably allow us to increase and integrate information to understand the causes and mechanisms of complex diseases. Oxidative stress is an etiological factor that influences numerous human diseases, including diabetes. C. elegans displays remarkably similar molecular bases and cellular pathways to those of mammals. Defects in the insulin/insulin-like growth factor-1 signaling pathway or increased ROS levels induce the conserved phase II detoxification response via the SKN-1 pathway to fight against oxidative stress. However, it is noteworthy that, aside from the detrimental effects of ROS, they have been proposed as second messengers that trigger the mitohormetic response to attenuate the adverse effects of oxidative stress. Herein, we briefly describe the importance of C. elegans as an experimental model system for studying metabolic disorders related to oxidative stress and the molecular mechanisms that underlie their pathophysiology.

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Effects of sod gene overexpression and deletion mutation on the expression profiles of reporter genes of major detoxification pathways in Caenorhabditis elegans

Cited by 46 publications

References 63 publications

Supplemental Cellular Protection by a Carotenoid Extends Lifespan via Ins/IGF-1 Signaling inCaenorhabditis elegans

Supplemental Cellular Protection by a Carotenoid Extends Lifespan via Ins/IGF-1 Signaling inCaenorhabditis elegans

Caffeic Acid Phenethylester Increases Stress Resistance and Enhances Lifespan in Caenorhabditis elegans by Modulation of the Insulin-Like DAF-16 Signalling Pathway

Caenorhabditis elegans: A Useful Model for Studying Metabolic Disorders in Which Oxidative Stress Is a Contributing Factor

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