High levels of p66shc and intracellular ROS in permanently arrested early embryos

Favetta, Laura A.; John, Elizabeth J. St.; King, W. A.; Betts, Dean H.

doi:10.1016/j.freeradbiomed.2007.01.018

Cited by 100 publications

(87 citation statements)

References 49 publications

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“…Again, this is contrary to our previous results for Day-8 parthenogenetic blastocysts, which show downregulated p53 expression [11]. Within IVF bovine embryos, the stress-related protein p66 shc is upregulated in early arrest, while p53 seems to not be involved in the same function [60][61][62]. In contrast, within embryos developed in the uterus, developmental arrest has been described as being both apoptosis-dependent [63] and apoptosis-independent [64].…”

Section: Gene Expression In Parthenotescontrasting

confidence: 99%

Gene Expression in Early Expanded Parthenogenetic and In Vitro Fertilized Bovine Blastocysts

Gómez

Caamaño

Bermejo-Álvarez³

et al. 2009

Journal of Reproduction and Development

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Abstract. Mammalian oocytes can undergo artificial parthenogenesis in vitro and develop to the blastocyst stage. In this study, using real-time PCR, we analyzed the expression of genes representative of essential events in development. In vitro matured oocytes were either fertilized or activated with ionomycin + 6-DMAP and cultured in simple medium. The pluripotency-related gene Oct3/4 was downregulated in parthenotes, while the de novo methylation DNMT3A gene was unchanged. Among the pregnancy recognition genes, IFN-t was upregulated, PGRMC1 was downregulated and PLAC8 was unchanged in parthenotes. Among the metabolism genes, SLC2A1 was downregulated, while AKR1B1, COX2, H6PD and TXN were upregulated in parthenotes; there was no difference in SLC2A5. Among the genes involved in compaction/blastulation, GJA1 expression increased in parthenotes, but no differences were detected within ATP1A1 and CDH1. Expression of p66 shc and the Bax/Bcl2 ratio were higher in parthenotes, and there was no difference in p53. Parthenotes and embryos may differ in the way they stimulate apoptosis, with a preponderant role for p66 shc within parthenotes. Differentially affected functions may also include pluripotency, de novo methylation and early embryonic signalling. Key words: Bovine, Embryo, Gene expression, Parthenote (J. Reprod. Dev. 55: [607][608][609][610][611][612][613][614] 2009) arthenogenesis, a form of reproduction not spontaneous in mammals, is a process by which the oocyte develops without the male gamete. Mammalian parthenotes are unable to develop to term in utero (developing for a maximum of 48 days in the cow; [1]), and this is thought to be due to alterations in their genomic imprinting, a mechanism that provides complementary, but not equivalent, specific expression between maternal and paternal genomes [2]. During fertilization, the spermatozoon triggers multiple and rhythmic oscillations of intracellular free calcium that release the oocyte from this blocked stage [3]. These intracellular calcium patterns can be mimicked by a number of chemicals that activate the oocyte without sperm, yielding parthenogenetic embryos [4]. In cattle, production of reconstructed embryos by somatic cell nuclear transfer (SCNT) [5] and intracytoplasmic sperm injection (ICSI) [6] depends on successful oocyte activation. Therefore, procedures involving SCNT and ICSI could benefit from a better knowledge of mechanisms that differ between embryos and parthenotes.Contrary to the research in mice and humans, most studies have failed to detect putatively imprinted genes in bovine early development [7,8], suggesting that monoallelic expression may not develop until after Day 21 of development, as occurs in ovine species [9]. In fact, a recent study found imprinted expression of bovine Mest-1 in Day-21 but not Day-14 embryos, while 7 other putatively imprinted genes were shown to be not imprinted at the two stages analyzed [10]. However, gene expression does differ between blastocysts from embryos and parthenotes in domestic species [11...

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Section: Gene Expression In Parthenotescontrasting

confidence: 99%

Gene Expression in Early Expanded Parthenogenetic and In Vitro Fertilized Bovine Blastocysts

Gómez

Caamaño

Bermejo-Álvarez³

et al. 2009

Journal of Reproduction and Development

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“…Higher level of apoptosis can also cause the loss of cell function, embryo fragmentation, and eventually embryonic arrest (Ahn et al, 2002;Favetta et al, 2007;Yoneda et al, 2004). The total cell number and the apoptotic index are suggested to be important indicators of embryo quality; previous study demonstrated that embryos with a greater number of cells are more likely to implant and to develop into live offspring (Van Soom et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Effect of peroxiredoxin II on the quality and mitochondrial activity of pre-implantation bovine embryos

Fakruzzaman

Ghanem

Bang

et al. 2015

Animal Reproduction Science

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“…Oxygen free radical damage to cellular components occurs, and to some extent, accumulates in living cells (Holmes et al 1992). We previously shown that simply varying the oxygen concentration of the culture environment alters the generation of reactive oxygen species and resultant oxidative damage in cells and embryos cultured in vitro (Favetta et al 2004;Favetta et al 2007). Mild chronic oxidative stress not only shortens the replicative capacity of cells but also increases the rate of telomere shortening proportionally (Duan et al 2005;Kurz et al 2004;von Zglinicki et al 1995).…”

Section: Discussionmentioning

confidence: 99%

Low oxygen delays fibroblast senescence despite shorter telomeres

2007

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It has been widely accepted that telomere shortening acts as a cell division counting mechanism that beyond a set critical length signals cells to enter replicative senescence. In this study, we demonstrate that by simply lowering the oxygen content of the cell culture environment 10-fold (20-2%) extends the replicative lifespan of fetal bovine fibroblasts at least five-times (30-150 days). Although, low oxygen fibroblasts display a slightly slower rate (P > 0.05) of telomere attrition than their high oxygen counterparts (171 bp versus 182 bp/PD), late passage fibroblasts (>50 PD) that have extended their replicative capacity under low oxygen conditions exhibited significantly (P < 0.05) shorter telomere lengths (11,135 +/- 467 bp) compared to senescent cells (25-34 PD) cultured under high oxygen conditions (14,827 +/- 1173 bp). There was a significant increase (P < 0.05) in chromosomal abnormalities with continual cell division under both high and low oxygen environments, however, fibroblasts displayed a significant reduction (P < 0.001) in chromosomal abnormalities at low oxygen tensions compared to those under 20% oxygen. These apparent protective effects on telomere shortening, delayed senescence and reduced chromosomal aberrations may be attributed to the up-regulation of telomerase activity observed for fibroblasts cultured under low oxygen. These results are consistent with the idea that a critically short telomere length may not be the sole trigger of replicative senescence, but may be regulated by the integrity of telomere structure itself and/or the amount of oxidative DNA damage in the cell.

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High levels of p66shc and intracellular ROS in permanently arrested early embryos

Cited by 100 publications

References 49 publications

Gene Expression in Early Expanded Parthenogenetic and In Vitro Fertilized Bovine Blastocysts

Gene Expression in Early Expanded Parthenogenetic and In Vitro Fertilized Bovine Blastocysts

Effect of peroxiredoxin II on the quality and mitochondrial activity of pre-implantation bovine embryos

Low oxygen delays fibroblast senescence despite shorter telomeres

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