O-linked N-acetyl-glucosamine deposition in placental proteins varies according to maternal glycemic levels

Justina, Vanessa Dela; Junior, Rinaldo Rodrigues dos Passos; Bressan, Alecsander F.; Tostes, Rita C.; Carneiro, Fernando S.; Soares, Thelma Shirlen; Volpato, Gustavo Tadeu; Lima, Victor Vitorino; Martín, Sebastián San; Giachini, Fernanda R.

doi:10.1016/j.lfs.2018.05.013

Cited by 15 publications

(17 citation statements)

References 41 publications

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“…No changes in OGT were observed during severe or mild hyperglycemia. O -GlcNAc overexpression in hyperglycemic conditions co-exist with placental dysfunction, which was characterized by morphometric alterations along with reduced placental index ( Dela Justina et al, 2018 ).…”

Section: O- Glcnac During Pregnancymentioning

confidence: 99%

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

et al. 2018

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Successful placentation is a key event for fetal development, which commences following embryo implantation into the uterine wall, eliciting decidualization, placentation, and remodeling of blood vessels to provide physiological exchange between embryo-fetus and mother. Several signaling pathways are recruited to modulate such important processes and specific proteins that regulate placental function are a target for the glycosylation with O-linked β-N-acetylglucosamine (O-GlcNAc), or O-GlcNAcylation. This is a reversible post-translational modification on nuclear and cytoplasmic proteins, mainly controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). O-GlcNAcylation has been implicated as a modulator of proteins, both in physiological and pathological conditions and, more recently, O-GlcNAc has also been shown to be an important modulator in placental tissue. In this mini-review, the interplay between O-GlcNAcylation of proteins and placental function will be addressed, discussing the possible implications of this post-translational modification through placental development and pregnancy.

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Section: O- Glcnac During Pregnancymentioning

confidence: 99%

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

et al. 2018

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“…This finding correlates with the reduced fetal vascular density in the labyrinth upon NK depletion and with the inflammatory status due to the increased NK cell density in the mesometrial lymphoid aggregate of pregnancy (13). Interestingly, changes in the glycosylation status predominantly affecting the placental labyrinth and junctional zone have been reported in a rat model of hyperglycemic placental dysfunction (46,47); suggesting that glycovariations in these layers induced by adverse maternal environments may have direct impact on placental function.…”

Section: Pre-placentation Manipulation Of the Relative Nk Cell-dc Abumentioning

confidence: 65%

Altered Glycosylation Contributes to Placental Dysfunction Upon Early Disruption of the NK Cell-DC Dynamics

et al. 2020

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“…As an X-linked gene and having the ability to transmit nutritional information to the nucleus, OGT is a unique candidate to signal maternal stress through the placenta to the developing fetus in a sex-dependent manner. Interestingly, O-GlcNAcylation of placental proteins correlates with maternal glycemic index (Dela Justina et al, 2018). In fact, a genome-wide screen looking for sex-specific changes in placental transcription after exposure to early prenatal stress identified Ogt as a top candidate for exhibiting sexually dimorphic expression in the placenta and changes in expression as a response to maternal stress (Howerton et al, 2013).…”

Section: Placental Ogt As a Biomarker For Neurodevelopmental Disease:mentioning

confidence: 99%

O-GlcNAc: Regulator of Signaling and Epigenetics Linked to X-linked Intellectual Disability

et al. 2020

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Cellular identity in multicellular organisms is maintained by characteristic transcriptional networks, nutrient consumption, energy production and metabolite utilization. Integrating these cell-specific programs are epigenetic modifiers, whose activity is often dependent on nutrients and their metabolites to function as substrates and co-factors. Emerging data has highlighted the role of the nutrient-sensing enzyme O-GlcNAc transferase (OGT) as an epigenetic modifier essential in coordinating cellular transcriptional programs and metabolic homeostasis. OGT utilizes the end-product of the hexosamine biosynthetic pathway to modify proteins with O-linked β-D-N-acetylglucosamine (O-GlcNAc). The levels of the modification are held in check by the O-GlcNAcase (OGA). Studies from model organisms and human disease underscore the conserved function these two enzymes of O-GlcNAc cycling play in transcriptional regulation, cellular plasticity and mitochondrial reprogramming. Here, we review these findings and present an integrated view of how O-GlcNAc cycling may contribute to cellular memory and transgenerational inheritance of responses to parental stress. We focus on a rare human genetic disorder where mutant forms of OGT are inherited or acquired de novo. Ongoing analysis of this disorder, OGT- X-linked intellectual disability (OGT-XLID), provides a window into how epigenetic factors linked to O-GlcNAc cycling may influence neurodevelopment.

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O-linked N-acetyl-glucosamine deposition in placental proteins varies according to maternal glycemic levels

Cited by 15 publications

References 41 publications

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

Altered Glycosylation Contributes to Placental Dysfunction Upon Early Disruption of the NK Cell-DC Dynamics

O-GlcNAc: Regulator of Signaling and Epigenetics Linked to X-linked Intellectual Disability

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