Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F24%3A10483944" target="_blank" >RIV/00179906:_____/24:10483944 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11150/24:10483944
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=2-4thVyLiV" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=2-4thVyLiV</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.ajpath.2023.12.011" target="_blank" >10.1016/j.ajpath.2023.12.011</a>
Alternative languages
Result language
angličtina
Original language name
Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes
Original language description
Preterm, prelabor rupture of the human fetal membranes (pPROM) is involved in 40% of spontaneous preterm births worldwide. Cellular-level disturbances and inflammation are effectors of membrane degradation, weakening, and rupture. Maternal risk factors induce oxidative stress (OS), senescence, and senescence-associated inflammation of the fetal membranes as reported mechanisms related to pPROM. Inflammation can also arise in fetal membrane cells (amnion/chorion) due to OS-induced autophagy and epithelial-mesenchymal transition (EMT). Autophagy, EMT, and their correlation in pPROM, along with OS-induced autophagy-related changes in amnion and chorion cells in vitro, were chymal marker) and proautophagy-inducing factor LC3B were performed in fetal membranes from pPROM, term not in labor, and term labor. Ultrastructural changes associated with autophagy were verified by transmission electron microscopy of the fetal membranes and in cells exposed to cigarette smoke extract (an OS inducer). EMT and LC3B staining was compared in the chorion from pPROM versus term not in labor. Transmission electron microscopy confirmed autophagosome formation in pPROM amnion and chorion. In cell culture, autophagosomes were formed in the amnion with OS treatment, while autophagosomes were accumulated in both cell types with autophagy inhibition. This study documents the association between pPROMs and amniochorion autophagy and EMT, and supports a role for OS in inducing dysfunctional cells that increase inflammation, predisposing membranes to rupture.
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
30214 - Obstetrics and gynaecology
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
American Journal of Pathology
ISSN
0002-9440
e-ISSN
1525-2191
Volume of the periodical
194
Issue of the periodical within the volume
5
Country of publishing house
US - UNITED STATES
Number of pages
9
Pages from-to
684-692
UT code for WoS article
001287268900001
EID of the result in the Scopus database
2-s2.0-85190444497