Thioredoxin-2 Modulates Neuronal Programmed Cell Death in the Embryonic Chick Spinal Cord in Basal and Target-Deprived Conditions

Pirson, Marc; Debrulle, Stéphanie; Clippe, André; Clotman, Frédéric; Knoops, Bernard

doi:10.1371/journal.pone.0142280

Cited by 4 publications

(7 citation statements)

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“…In addition to being interesting from an evolutionary standpoint, the absence of PRDX5 in birds also offers the opportunity to develop several gain-of-function models to study PRDX5. Though a cell culture approach through commonly used DT40 chicken B cell line could be envisioned, over the last decade, in ovo electroporation has been widely used for gain- or loss-of-function studies during chick embryonic development [ 26 , 68 ]. This is especially interesting in light of recent reports of a particular expression pattern of PRDX5 in the mouse embryonic spinal cord [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…Fertilized eggs were obtained from Wyverkens farm (Halle, Belgium). Animal and tissue processing was performed according to protocols described in Pirson and Knoops (2015) and Pirson et al (2015) [ 25 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

“…Western blotting of chicken tissue homogenate proteins and SH-SY5Y (human neuroblastoma) cell lysate proteins, serving as a positive control, was performed as previously described [ 25 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

“…Treatment of fertilized eggs and in ovo electroporation of chick embryos were performed as previously described [ 26 ]. Briefly, pCMS- eGFP vector (Empty vector), pCMS- eGFP vector with human L-PRDX5 ( L-PRDX5 vector) or S-PRDX5 ( S-PRDX5 vector) cDNA sequences were injected into the neural tube of Hamilton-Hamburger stage (HH) 12–14, i.e.…”

Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence assay and image acquisition of chick embryonic spinal cords was performed as previously described [ 25 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

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The curious case of peroxiredoxin-5: what its absence in aves can tell us and how it can be used

2018

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BackgroundPeroxiredoxins are ubiquitous thiol-dependent peroxidases that represent a major antioxidant defense in both prokaryotic cells and eukaryotic organisms. Among the six vertebrate peroxiredoxin isoforms, peroxiredoxin-5 (PRDX5) appears to be a particular peroxiredoxin, displaying a different catalytic mechanism, as well as a wider substrate specificity and subcellular distribution. In addition, several evolutionary peculiarities, such as loss of subcellular targeting in certain species, have been reported for this enzyme.ResultsWestern blotting analyses of 2-cys PRDXs (PRDX1–5) failed to identify the PRDX5 isoform in chicken tissue homogenates. Thereafter, via in silico analysis of PRDX5 orthologs, we went on to show that the PRDX5 gene is conserved in all branches of the amniotes clade, with the exception of aves. Further investigation of bird genomic sequences and expressed tag sequences confirmed the disappearance of the gene, though TRMT112, a gene located closely to the 5′ extremity of the PRDX5 gene, is conserved. Finally, using in ovo electroporation to overexpress the long and short forms of human PRDX5, we showed that, though the gene is lost in birds, subcellular targeting of human PRDX5 is conserved in the chick.ConclusionsFurther adding to the distinctiveness of this enzyme, this study reports converging evidence supporting loss of PRDX5 in aves. In-depth analysis revealed that this absence is proper to birds as PRDX5 appears to be conserved in non-avian amniotes. Finally, taking advantage of the in ovo electroporation technique, we validate the subcellular targeting of human PRDX5 in the chick embryo and bring forward this gain-of-function model as a potent way to study PRDX5 functions in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence assay and image acquisition of chick embryonic spinal cords was performed as previously described [ 25 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

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The curious case of peroxiredoxin-5: what its absence in aves can tell us and how it can be used

2018

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Overexpression of thioredoxin‐2 attenuates age‐related muscle loss by suppressing mitochondrial oxidative stress and apoptosis

Tang

Kim

Lee

et al. 2022

JCSM Rapid Communications

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Background Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age-dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin-2 (TXN2). Methods We tested the functional role of TXN2 using ageing (n = 7-10 per group) and denervation (n = 3 per group) models in a transgenic mouse line that overexpresses TXN2. We investigated if overexpression of TXN2 blocks muscle loss in these models by examination of muscle weight, fibre size, and fibre number in young (~7 months) and aged (~26 months) TXN2-transgenic mice and controls. We studied the underlying mechanisms by mRNA and protein assays including transcriptomic profiling, western blot analysis, immunostaining, as well as succinate dehydrogenase, dihydroethidium, and terminal deoxynucleotidyl transferase dUTP nick end labelling staining. Results Overexpression of TXN2 did not significantly alter the baseline skeletal muscle size, weight, fibre type distribution, or expression of mitochondrial respiratory chain components, but it did preserve muscle mass during ageing. The hindlimb muscle mass in aged TXN-transgenic mice was ~21-24% greater (in tibialis anterior, gastrocnemius/soleus combined, and tibialis anterior/extensor digitorum longus combined) than in age-matched controls (all P < 0.05). The reduction in both muscle fibre number (872 ± 206 vs, 637 ± 256 fibres in extensor digitorum longus muscle, P < 0.05) and muscle fibre size (1959 ± 296 vs. 1477 ± 564 μm 2 in tibialis anterior muscle, P < 0.05) seen in young vs. aged control muscles was not significant in young vs. aged TXN-transgenic mice (both P > 0.05). Transcriptomic analysis revealed that catabolic genes that are up-regulated in ageing muscle, including those subserving apoptosis and the ubiquitin-like conjugation system, were normalized by TXN2 overexpression. Further, overexpressing TXN2 suppressed oxidative stress and caspase-9/3-mediated apoptotic signalling in the aged muscle at the protein level. Although denervation and its effects have been considered a component of age-related muscle atrophy, TXN2 overexpression failed to attenuate atrophy in an acute denervation model (TXN-transgenic vs. control mice, P > 0.05), despite preventing denervation-induced oxidative stress and apoptosis. Conclusions Mitochondrial oxidative stress appears to play a crucial role in effecting chronic age-dependent, but not acute neurogenic, muscle atrophy. Increased TXN2 protects muscle against oxidative stress-associated catabolic activity in ageing muscle and thus is a potential therapeutic approach to attenuate age-related muscle atrophy.

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Effect of antioxidants on preimplantation embryo developmentin vitro: a review

Zarbakhsh

2021

Zygote

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Summary In vitro culture of the embryo is a useful method to treat infertility that shows embryo potential for selecting the best one to transfer and successfully implantation. However, embryo development in vitro is affected by oxidative stresses such as reactive oxygen species that may damage embryo development. Antioxidants are molecules found in fruits, vegetables, and fish that play an important role in reducing oxidative processes. In the natural environment, there is a physiological antioxidant system that protects embryos against oxidative damage. This antioxidant system does not exist in vitro. Antioxidants act as free radical scavengers and protect cells or repair damage done by free radicals. Various studies have shown that adding antioxidants into embryo culture medium improves embryo development in vitro. This review article emphasizes different aspects of various antioxidants, including types, functions and mechanisms, on the growth improvement of different species of embryos in vitro.

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Thioredoxin-2 Modulates Neuronal Programmed Cell Death in the Embryonic Chick Spinal Cord in Basal and Target-Deprived Conditions

Cited by 4 publications

References 54 publications

The curious case of peroxiredoxin-5: what its absence in aves can tell us and how it can be used

The curious case of peroxiredoxin-5: what its absence in aves can tell us and how it can be used

Overexpression of thioredoxin‐2 attenuates age‐related muscle loss by suppressing mitochondrial oxidative stress and apoptosis

Effect of antioxidants on preimplantation embryo developmentin vitro: a review

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