Differential senescence in feto-maternal tissues during mouse pregnancy
Open accessAbstract
Background Human studies show that fetal membranes have a limited lifespan and undergo telomere-dependent cellular senescence that is augmented by oxidative stress and mediated by p38 mitogen activated protein kinase (MAPK). Further, these studies suggest that fetal membranes are anatomically and physiologically positioned to transmit senescence signals that may initiate parturition at term.Methods Longitudinal evaluation of feto-maternal tissues from mouse pregnancies was undertaken to determine the molecular progression of senescence during normal pregnancy. On days 10-18 of gestation, C57BL/6 mice were euthanized. Fetal membranes, placenta, and decidua/uterus were collected. Tissues were examined for Telomere length (TL) and the presence of Phosphorylated (P) p38MAPK and p53, p21 and senescence associated β-Galactosidase (SA- β-Gal).Findings Linear regression modeling of observed telomere length as a function of gestational age revealed that beta (β), the slope of the linear regression was negative and significantly different from zero for each tissue (fetal membranes, β = -0.1901 ± 0.03125, p < 0.0001; placenta β = -0.09000 ± 0.03474, p = 0.0135; decidua/uterus β = -0.1317 ± 0.03264, p = 0.0003). Progressive activation p38MAPK was observed in all tissues from days 10 to day18, with the highest activation observed in fetal membranes. Activation of p53 was progressive in fetal membranes. In contrast, active p53 was constitutive in placenta and decidua/uterus throughout gestation. Detection of p21 indicated that pro-senescent change was higher in all compartments on day 18 as compared to other days. The number of SA-β-Gal positive cells increased in fetal membranes as gestation progressed. However, in placenta and uterus and decidua/uterus SA-β-Gal was seen only in days 15 and 18.Conclusions Telomere dependent p38 and p53 mediated senescence progressed in mouse fetal membranes as gestation advanced. Although senescence is evident, telomere dependent events were not dominant in placenta or decidua/uterus. Fetal membrane senescence may significantly contribute to mechanisms of parturition at term.
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Trophoblast senescence is physiological, progresses with gestation and peaks at term; senescence is also described in maternal decidual cells and fetoplacental membranes, where it promotes parturition and placental detachment at term.
“In addition to trophoblast senescence, which is a physiological phenomenon that progresses with gestation and peaks at term, senescence is also extensively described in maternal decidual cells and fetoplacental membranes, where it has a pivotal role in the promotion of parturition and detachment of the placenta from the uterus at term257–262.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [258]
The Discussion (page not provided) reports that fetal-membrane senescence progresses through mouse gestation, while placental and decidual senescence is minimal and detectable only near its end. The Conclusions say fetal-membrane senescence may contribute to parturition at term. The paper does not establish progressive senescence specifically in trophoblasts or a role for senescence in placental detachment, and the claim states the parturition role more definitively than the source does. (LLM, conf=0.88)
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References 58 · Cited by 86
Research works printed but not linked: 1
- [33]Gomez-Lopez N Olson DM Robertson SA Interleukin-6 controls uterine Th9 cells and CD8(+) T regulatory cells to accelerate parturition in mice Immunology and cell biology 2016 94 1 79 89 26073576
- Authors
- Bonney, E. A., Krebs, K., Saade, G., Kechichian, T., Trivedi, J., Huaizhi, Y., & Menon, R.
- Affiliations
- University of Vermont (US)
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Menon, Ramkumar
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 43
- Pages
- 26-34
- ISSN
- 0143-4004 (ISSN-L)
- PMC
- PMC5527294
- OpenAlex
- W2343363897
- Cited by
- 86
- References
- 58
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 6 · 2023: 10 · 2022: 8 · 2021: 6 · 2020: 11 · 2019: 13 · 2018: 7 · 2017: 14 · 2016: 2
- FWCI
- 9.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Department of Obstetrics, Gynecology and Reproductive Sciences, University of Vermont College of Medicine
- Department of OB & GYN, The University of Texas Medical Branch
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Keywords
- senescence, cellular senescence, telomere length, p38 MAPK, p53, p21, senescence-associated β-galactosidase, decidua, uterine tissue, fetal membranes, mouse pregnancy, gestational age, oxidative stress, childbirth
- MeSH terms
- Animals, Decidua, Female, Extraembryonic Membranes, Gestational Age, Mice, Inbred C57BL, Phosphorylation, Placenta, Pregnancy, Tumor Suppressor Protein p53, Telomere, Cellular Senescence, Oxidative Stress, p38 Mitogen-Activated Protein Kinases, Mice
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