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Fetal Growth Restriction is Associated with Accelerated Telomere Shortening and Increased Expression of Cell Senescence Markers in the Placenta
Open accessAbstract
A hallmark of fetal growth restriction (FGR) is restricted placental development and insufficient nutrient supply to the fetus. It has previously been shown that activity levels of telomerase, the enzyme responsible for completing replication of telomeric DNA during cell division, is suppressed in FGR placenta samples as compared to control placenta samples from donors of the same gestational age. Here we examine whether telomere length maintenance is also compromised in FGR placenta samples. Southern analysis of telomere length for placenta and cord blood samples from 32 FGR and 36 control donors, ranging in gestational age from 37 to 40 weeks, revealed significantly shorter telomeres (P<or=0.001) in FGR placenta samples, but not cord blood samples. Furthermore, analysis of telomerase extracts, RNA and DNA placental samples from donors with and without idiopathic FGR confirmed a direct association between suppression of telomerase activity and reduced telomere length in FGR placenta. In addition, expression levels of markers of telomere-induced senescence, p21, p16 and EF-1 alpha, were significantly elevated in FGR placenta samples (P<or=0.01). These observations support a direct affect of reduced telomerase activity levels on the placental pathology associated with FGR.
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“Telomeres from fetal growth restriction placentas are shorter and express higher levels of CDKN2A and CDKN1A protein and EEF1A1 RNA compared with placentas from normal growth fetuses265.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [265]
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1 of the 21 references couldn’t be matched to a known paper.
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- Bianchi, 2000, Chapter 124: intrauterine growth restriction
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SenNet recommendations for detecting senescent cells in different tissues
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“Telomeres from fetal growth restriction placentas are shorter and express higher levels of CDKN2A and CDKN1A protein and EEF1A1 RNA compared with placentas from normal growth fetuses 265 .”
Placental Apoptosis in Health and Disease
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Joo, E. H., Kim, Y. R., Kim, N., Jung, J. E., Han, S. H., & Cho, H. Y. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221810122 · Cited by 217
Metadata
- Authors
- Davy, P., Nagata, M., Bullard, P., Fogelson, N. S., & Allsopp, R.
- Affiliations
- University of Hawaiʻi at Mānoa (US)
- Corresponding author
- Allsopp, R.
- ORCID
- Venue
- Placenta
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 30
- Issue
- 6
- Pages
- 539-542
- ISSN
- 0143-4004 (ISSN-L)
- PMC
- PMC2692289
- OpenAlex
- W2048877882
- Cited by
- 137
- References
- 21
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 5 · 2023: 16 · 2022: 10 · 2021: 8 · 2020: 9 · 2019: 8 · 2018: 10 · 2017: 15 · 2016: 12 · 2015: 7 · 2014: 8 · 2013: 3 · 2012: 6
- FWCI
- 6.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Placenta (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5p20rr011091-15)
- National Center for Research Resources (P20-RR011091)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Keywords
- fetal growth restriction, telomere shortening, telomerase activity, cellular senescence, p21, p16, EF-1α, umbilical cord blood, placental development
- MeSH terms
- Adolescent, Adult, Female, Fetal Growth Retardation, Humans, Infant, Newborn, Middle Aged, Pregnancy, Biomarkers, Up-Regulation, Case-Control Studies, Telomere, Cellular Senescence, Chromosomal Instability, Young Adult
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