Expression of Apoptosis in Placentae from Mice Lacking the Prostaglandin F Receptor
Abstract
This study aimed to investigate the changes in apoptosis in the placenta and decidua of pregnant mice lacking the prostaglandin F receptor. Mouse placentae were removed from fetuses on days 10-23 of pregnancy. Apoptotic cells were examined by a DNA fragmentation assay and the terminal deoxynucleotidyl transferase-mediated dUDP nick end-labelling (TUNEL) technique. The placenta and decidual weight increased before day 18 and 14 of pregnancy, and then decreased with gestational day. After day 19, the fetuses gradually died in the uterus. All fetuses died in the uterus on day 23 of pregnancy. The number of apoptosis was not significantly different between wild type and FP-deficient mice before day 18 of pregnancy by DNA fragmentation and TUNEL staining. The DNA fragmentation was always more pronounced in decidual tissue on each day of pregnancy. DNA laddering on placentae was more extensive on day 22 than day 18. In placenta, most TUNEL-positive cells were detected in trophoblast and stromal cells. A higher intensity of apoptotic cells was in the decidual basalis. The main area was the centre of the decidual basalis, and was in decrease toward to margin of placenta. The index of TUNEL positive cells increased as gestation progressed toward termination. Especially, it was prominent in the placentae on day 22 compared with that day 18 of pregnancy. The increased TUNEL-positive staining in syncytiotrophoblast surface was found in placenta at post-term, compared with those at term. Apoptosis may provide insights into both normal placental development and placental dysfunction during an abnormal pregnancy from post-term pregnancy.
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Apoptosis at the decidual/uterine interface allows initial separation of the maternal/placental unit at the time of parturition.
“putatively allowing for initial separation of the maternal/placental unit at the time of parturition40–43.”
From Conditional loss of ERK1 and ERK2 results in abnormal placentation and delayed parturition in the mouse (2019) · cites this paper as [42]
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- Authors
- Mu, J., Kanzaki, T., Tomimatsu, T., Fukuda, H., Wasada, K., Fujii, E., Endoh, M., Kozuki, M., Murata, Y., Sugimoto, Y., & Ichikawa, A.
- Affiliations
- The University of Osaka (JP)
- Kyoto University (JP)
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2002-02
- Volume
- 23
- Issue
- 2-3
- Pages
- 215-223
- ISSN
- 0143-4004 (ISSN-L)
- OpenAlex
- W2151314502
- Cited by
- 26
- References
- 36
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 1 · 2020: 2 · 2019: 3 · 2017: 2 · 2016: 1 · 2015: 2 · 2013: 1
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Agricultural and Biological Sciences › Agronomy and Crop Science › Reproductive Physiology in Livestock
- Keywords
- apoptosis, prostaglandin F receptor, decidua, trophoblast, syncytiotrophoblast, placental development, prolonged pregnancy, placental insufficiency, abortion, DNA fragmentation, TUNEL staining
- MeSH terms
- Animals, Cell Count, Decidua, DNA, Female, Male, Organ Size, Placenta, Pregnancy, Receptors, Prostaglandin, Apoptosis, Mice, Knockout, In Situ Nick-End Labeling, Mice, DNA Fragmentation
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