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Ramkumar Menon 대한산부인과학회 2019 Obstetrics & Gynecology Science Vol.62 No.4
A better understanding of the underlying mechanisms by which signals from the fetus initiate human parturitionis required. Our recent findings support the core hypothesis that oxidative stress (OS) and cellular senescence ofthe fetal membranes (amnion and chorion) trigger human parturition. Fetal membrane cell senescence at term is anatural physiological response to OS that occurs as a result of increased metabolic demands by the maturing fetus. Fetal membrane senescence is affected by the activation of the p38 mitogen activated kinase-mediated pathway. Similarly, various risk factors of preterm labor and premature rupture of the membranes also cause OS-inducedsenescence. Data suggest that fetal cell senescence causes inflammatory senescence-associated secretory phenotype(SASP) release. Besides SASP, high mobility group box 1 and cell-free fetal telomere fragments translocate from thenucleus to the cytosol in senescent cells, where they represent damage-associated molecular pattern markers (DAMPs). In fetal membranes, both SASPs and DAMPs augment fetal cell senescence and an associated ‘sterile’ inflammatoryreaction. In senescent cells, DAMPs are encapsulated in extracellular vesicles, specifically exosomes, which are 30–150nm particles, and propagated to distant sites. Exosomes traffic from the fetus to the maternal side and cause laborassociatedinflammatory changes in maternal uterine tissues. Thus, fetal membrane senescence and the inflammationgenerated from this process functions as a paracrine signaling system during parturition. A better understandingof the premature activation of these signals can provide insights into the mechanisms by which fetal signals initiatepreterm parturition.
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Ramkumar Menon 생화학분자생물학회 2022 BMB Reports Vol.55 No.8
Human pregnancy is a delicate and complex process wheremultiorgan interactions between two independent systems, themother, and her fetus, maintain pregnancy. Intercellular interactionsthat can define homeostasis at the various cellular levelbetween the two systems allow uninterrupted fetal growth anddevelopment until delivery. Interactions are needed for tissueremodeling during pregnancy at both fetal and maternal tissuelayers. One of the mechanisms that help tissue remodeling isvia cellular transitions where epithelial cells undergo a cyclictransition from epithelial to mesenchymal (EMT) and back frommesenchymal to epithelial (MET). Two major pregnancy-associatedtissue systems that use EMT, and MET are the fetal membrane(amniochorion) amnion epithelial layer and cervical epithelialcells and will be reviewed here. EMT is often associatedwith localized inflammation, and it is a well-balanced processto facilitate tissue remodeling. Cyclic transition processes areimportant because a terminal state or the static state of EMTcan cause accumulation of proinflammatory mesenchymal cellsin the matrix regions of these tissues and increase localizedinflammation that can cause tissue damage. Interactions thatdetermine homeostasis are often controlled by both endocrineand paracrine mediators. Pregnancy maintenance hormoneprogesterone and its receptors are critical for maintaining thebalance between EMT and MET. Increased intrauterine oxidativestress at term can force a static (terminal) EMT and increaseinflammation that are physiologic processes that destabilizehomeostasis that maintain pregnancy to promote labor and deliveryof the fetus. However, conditions that can produce anuntimely increase in EMT and inflammation can be pathologic. These tissue damages are often associated with adverse pregnancycomplications such as preterm prelabor rupture of themembranes (pPROM) and spontaneous preterm birth (PTB). Therefore, an understanding of the biomolecular processes thatmaintain cyclic EMT-MET is critical to reducing the risk ofpPROM and PTB. Extracellular vesicles (exosomes of 40-160nm) that can carry various cargo are involved in cellular transitionsas paracrine mediators. Exosomes can carry a variety ofbiomolecules as cargo. Studies specifically using exosomes fromcells undergone EMT can carry a pro-inflammatory cargo andin a paracrine fashion can modify the neighboring tissue environmentto cause enhancement of uterine inflammation.
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