Telomere homeostasis in IUGR placentas – A review

Biron‐Shental, Tal; Sadeh-Mestechkin, Dana; Amiel, Aliza

doi:10.1016/j.placenta.2015.11.006

Cited by 23 publications

(25 citation statements)

References 38 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 including stillbirth, spontaneous preterm labor, poorly controlled maternal diabetes, pre‐eclampsia and FGR. Previous studies in placentas of pregnancies complicated by FGR showed markers of placental aging, including shorter telomeres, telomerase activity suppression and increased apoptosis mediated by the p53 pathway. However, it is unclear whether SGA pregnancies with apparently normal placental function on ultrasound examination have significant placental aging or if this phenomenon is restricted solely to fetuses with FGR.…”

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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“…Placental bed biopsies from cases of IUGR indeed show a reduction in dNK cells (Williams et al , ). In addition, IUGR placentas exhibit increased signs of impaired telomere homeostasis (Davy et al , ; Biron‐Shental et al , , ). It is possible that the cytotrophoblast cell population undergo increased proliferation as a compensatory mechanism to maintain the integrity of compromised syncytiotrophoblast.…”

Section: Discussionmentioning

confidence: 99%

Molecular pathways of senescence regulate placental structure and function

et al. 2019

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The placenta is an autonomous organ that maintains fetal growth and development. Its multinucleated syncytiotrophoblast layer, providing fetal nourishment during gestation, exhibits characteristics of cellular senescence. We show that in human placentas from pregnancies with intrauterine growth restriction, these characteristics are decreased. To elucidate the functions of pathways regulating senescence in syncytiotrophoblast, we used dynamic contrast‐enhanced MRI in mice with attenuated senescence programs. This approach revealed an altered dynamics in placentas of p53−/−, Cdkn2a−/−, and Cdkn2a−/−;p53−/− mice, accompanied by histopathological changes in placental labyrinths. Human primary syncytiotrophoblast upregulated senescence markers and molecular pathways associated with cell‐cycle inhibition and senescence‐associated secretory phenotype. The pathways and components of the secretory phenotype were compromised in mouse placentas with attenuated senescence and in human placentas from pregnancies with intrauterine growth restriction. We propose that molecular mediators of senescence regulate placental structure and function, through both cell‐autonomous and non‐autonomous mechanisms.

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“…Trophoblasts mimic cancer cells by displaying invasiveness in order to support growth of the fetus. Like neoplastic cells, trophoblasts maintain their telomere length and Human Telomerase Reverse Transcriptase (hTERT) level in uncomplicated pregnancies [83, 84]. During the first trimester, the trophoblast experiences low oxygen tension or a physiologic hypoxic state, associated with the upregulation of HIF-1 α .…”

Section: Cellular Senescence In Adverse Pregnancy Outcomesmentioning

confidence: 99%

“…The telomere length remains constant throughout normal pregnancy, but in certain conditions like fetal growth restriction and uncontrolled diabetes, telomere length is significantly reduced [88, 89]. Telomere changes could be associated with increased oxidative stress, leading to DNA damage and activation of damage response (DDR) through the p53 pathway and promoting senescence of the trophoblast [9, 84]. In 2010, Biron-Shental et al were the first to report evidence of cellular senescence in preeclampsia and fetal growth restriction.…”

Section: Cellular Senescence In Adverse Pregnancy Outcomesmentioning

confidence: 99%

Placental Ageing in Adverse Pregnancy Outcomes: Telomere Shortening, Cell Senescence, and Mitochondrial Dysfunction

Manna

McCarthy

2019

Oxidative Medicine and Cellular Longevity

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Preeclampsia is a multisystemic pregnancy disorder and a major cause of maternal and neonatal morbidity and mortality worldwide. The exact pathophysiology of preeclampsia remains unclear; however, it is speculated that the various pathologies can be attributed to impaired vascular remodelling and elevated oxidative stress within the placenta. Oxidative stress plays a key role in cell ageing, and the persistent presence of elevated oxidative stress precipitates cellular senescence and mitochondrial dysfunction, resulting in premature ageing of the placenta. Premature ageing of the placenta is associated with placental insufficiency, which reduces the functional capacity of this critical organ and leads to abnormal pregnancy outcomes. The changes brought about by oxidative insults are irreversible and often lead to deleterious modifications in macromolecules such as lipids and proteins, DNA mutations, and alteration of mitochondrial functioning and dynamics. In this review, we have summarized the current knowledge of placental ageing in the aetiology of adverse pregnancy outcomes and discussed the hallmarks of ageing which could be potential markers for preeclampsia and fetal growth restriction.

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Telomere homeostasis in IUGR placentas – A review

Cited by 23 publications

References 38 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

Molecular pathways of senescence regulate placental structure and function

Placental Ageing in Adverse Pregnancy Outcomes: Telomere Shortening, Cell Senescence, and Mitochondrial Dysfunction

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