Impact of antiphospholipid syndrome on placenta and uterine NK cell function: insights from a mouse model
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00098892%3A_____%2F24%3A10158895" target="_blank" >RIV/00098892:_____/24:10158895 - isvavai.cz</a>
Alternative codes found
RIV/61989592:15110/24:73627310 RIV/61989100:27240/24:10256979
Result on the web
<a href="https://www.nature.com/articles/s41598-024-82451-2" target="_blank" >https://www.nature.com/articles/s41598-024-82451-2</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41598-024-82451-2" target="_blank" >10.1038/s41598-024-82451-2</a>
Alternative languages
Result language
angličtina
Original language name
Impact of antiphospholipid syndrome on placenta and uterine NK cell function: insights from a mouse model
Original language description
Antiphospholipid syndrome (APS) is associated with recurrent pregnancy morbidity, yet the underlying mechanisms remain elusive. We performed multifaceted characterization of the biological and transcriptomic signatures of mouse placenta and uterine natural killer (uNK) cells in APS. Histological analysis of APS placentas unveiled placental abnormalities, including disturbed angiogenesis, occasional necrotic areas, fibrin deposition, and nucleated red blood cell enrichment. Analyses of APS placentas showed a reduced cell proliferation, lower protein content and thinning of endothelial cells. Disturbances in APS trophoblast cells were linked to a cell cycle shift in cytotrophoblast cells, and a reduced number of spiral artery-associated trophoblast giant cells (SpA-TGC). Transcriptomic profiling of placental tissue highlighted disruptions in cell cycle regulation with notable downregulation of genes involved in developmental or signaling processes. Cellular senescence, metabolic and p53-related pathways were also enriched, suggesting potential mechanisms underlying placental dysfunction in APS. Thrombotic events, though occasionally detected, appeared to have no significant impact on the overall pathological changes. The increased number of dysfunctional uNK cells was not associated with enhanced cytotoxic capabilities. Transcriptomic data corroborated these findings, showing prominent suppression of NK cell secretory capacity and cytokine signaling pathways. Our study highlights the multifactorial nature of APS-associated placental pathologies, which involve disrupted angiogenesis, cell cycle regulation, and NK cell functionality.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30102 - Immunology
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2024
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Scientific Reports
ISSN
2045-2322
e-ISSN
2045-2322
Volume of the periodical
14
Issue of the periodical within the volume
1
Country of publishing house
DE - GERMANY
Number of pages
15
Pages from-to
31163
UT code for WoS article
001385898400043
EID of the result in the Scopus database
2-s2.0-85213516977