Is there a role for placental senescence in the genesis of obstetric complications and fetal growth restriction?

Sultana, Zakia; Maiti, Kaushik; Dedman, Lee; Smith, Roger

doi:10.1016/j.ajog.2017.11.567

Cited by 107 publications

(80 citation statements)

References 134 publications

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“…Our results suggesting premature placental aging in small fetuses are consistent with those of previous studies showing reduced telomerase activity, shorter telomeres 23,30,32,46 and increased expression of cell senescence markers (p21, p16 and EF-1α) in the placenta of pregnancies with a small fetus 34 . Telomeres are nucleoprotein structures located at the termini of chromosomes that become progressively shorter in each mitotic cycle or due to environmental factors.…”

Section: Discussionsupporting

confidence: 92%

“…Altered placental aging has been described in several obstetric complications 23 including stillbirth 24,25 , spontaneous preterm labor [26][27][28] , poorly controlled maternal diabetes 29 , pre-eclampsia and FGR 30,31 . Previous studies in placentas of pregnancies complicated by FGR showed markers of placental aging, including shorter telomeres, telomerase activity suppression [32][33][34] and increased apoptosis mediated by the p53 pathway [35][36][37] .…”

Section: Introductionmentioning

confidence: 99%

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Premature placental aging in term small‐for‐gestational‐age and growth‐restricted fetuses

Paulés

Dantas

Miranda

et al. 2019

Ultrasound in Obstet & Gyne

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Premature placental aging in term small‐for‐gestational‐age and growth‐restricted fetuses

Paulés

Dantas

Miranda

et al. 2019

Ultrasound in Obstet & Gyne

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“…Moreover, acute atherosis has been linked to increased oxidative stress and lipid content in the decidua of preeclamptic women . Oxidative stress is also implicated in the pathophysiology of preeclampsia and fetal growth restriction . Hence, we proposed that macrophages are implicated in the mechanisms leading to oxidative stress, and therefore, obstetrical disease (ie, acute atherosis).…”

Section: Discussionmentioning

confidence: 99%

The immunophenotype of decidual macrophages in acute atherosis

Gill

Leng

Romero

et al. 2019

American J Rep Immunol

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Problem: Acute atherosis is a uteroplacental arterial lesion that is associated with pregnancy complications such as preeclampsia and preterm birth, the latter being the leading cause of perinatal morbidity and mortality worldwide. However, the immunobiology of acute atherosis is poorly understood. Method of study:Placental basal plate samples were collected from women who delivered with (n = 11) and without (n = 31) decidua basalis lesions of acute atherosis.Multicolor flow cytometry was used to quantify M1-and M2-like macrophage subsets and the expression of iNOS and IL-12 by decidual macrophages. Multiplex fluorescence staining and phenoptics were performed to localize M1-, MOX-, and Mhem-like macrophages in the decidual basalis. Results:Macrophages displayed diverse phenotypes in the decidua basalis with acute atherosis. M2-like macrophages were the most abundant subset in the decidua; yet, this macrophage subset did not change with the presence of acute atherosis. Decidual M1-like macrophages were increased in acute atherosis, and such macrophages displayed a pro-inflammatory phenotype, as indicated by the expression of iNOS and IL-12. Decidual M1-like pro-inflammatory macrophages were localized near both transformed and non-transformed vessels in the decidua basalis with acute atherosis.

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“…Both DNA damage and oxidative stress are able to induce cellular senescence. Two pathways both initiate and maintain cellular senescence, the p53-p21-pRB and the p16-pRB pathways (Sultana et al, 2018). Induction of either of these converging pathways results in cell cycle arrest.…”

Section: Introductionmentioning

confidence: 99%

Loss of SATB1 Induces a p21 Dependent Cellular Senescence Phenotype in Dopaminergic Neurons

Rießland

Kolisnyk

et al. 2018

Preprint

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Cellular senescence is a mechanism used by mitotic cells to prevent uncontrolled cell division. As senescent cells persist in tissues, they cause local inflammation and are harmful to surrounding cells, contributing to aging. Generally, neurodegenerative diseases, such as Parkinson's, are disorders of aging. The contribution of cellular senescence to neurodegeneration is still unclear. SATB1 is a DNA binding protein associated with Parkinson's disease. We report that SATB1 prevents cellular senescence in post-mitotic dopaminergic neurons. Loss of SATB1 causes activation of a cellular senescence transcriptional program in dopamine neurons, both in human stem cell-derived dopaminergic neurons and in mice. We observed phenotypes which are central to cellular senescence in SATB1 knockout dopamine neurons in vitro and in vivo. Moreover, we found that SATB1 directly represses expression of the pro-senescence factor, p21, in dopaminergic neurons. Our data implicate senescence of dopamine neurons as a contributing factor to the pathology of Parkinson's disease. hESC shows normal appearance. Scale bar: 200 µm. (D) Immunolabeling of DA precursor markers in WT and SATB1 KO hESC derived DA neurons after 16 days of differentiation reveals no difference in marker expression. (E) Depiction of spontaneous action potentials of WT and SATB1 KO DA neurons at different time points show that both genotypes differentiate into mature DA neurons between day 35 and 40. Scale bar: 20 mV, 2 s. (F) DA neurons at day 40 show significant differences in maintenance of response to positive current injections. Scale bar: 20 mV, 200 ms. (G) Longitudinal comparison of cell survival of WT vs. SATB1 KO DA neurons revealed a significant reduction in SATB1 KO survival between day 30 and 40, reaching a plateau at ~50%. Data are represented as mean ± SEM. (H) Quantification of neurite morphology and complexity in WT and SATB1 KO DA neurons. Data are represented as mean ± SEM. (I) Triple immunolabeling of cortical shows that both WT as well as SATB1 KO neurons express the essential markers for cortical neurons. Scale bar: 50 µm. (J) SATB1 KO cortical neurons show no significant change in survival during differentiation. Data are represented as mean ± SEM. (K) Quantification of neurite morphology and complexity in WT and SATB1 KO CTX neurons. (L)Representative western blot and quantification depicts that WT DA neurons express significantly higher levels of SATB1 than WT cortical neurons, suggesting a higher demand in DA neurons. Data are represented as mean ± SEM. See also Figure S1.

show abstract

Is there a role for placental senescence in the genesis of obstetric complications and fetal growth restriction?

Cited by 107 publications

References 134 publications

Premature placental aging in term small‐for‐gestational‐age and growth‐restricted fetuses

Premature placental aging in term small‐for‐gestational‐age and growth‐restricted fetuses

The immunophenotype of decidual macrophages in acute atherosis

Loss of SATB1 Induces a p21 Dependent Cellular Senescence Phenotype in Dopaminergic Neurons

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