Placental mediated mechanisms of perinatal brain injury: Evolving inflammation and exosomes.

Autor: Gall AR; Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Amoah S; Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Kitase Y; Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Jantzie LL; Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Kennedy Krieger Institute, Baltimore, MD, USA. Electronic address: LJantzie@jhmi.edu.
Jazyk: angličtina
Zdroj: Experimental neurology [Exp Neurol] 2022 Jan; Vol. 347, pp. 113914. Date of Electronic Publication: 2021 Nov 06.
DOI: 10.1016/j.expneurol.2021.113914
Abstrakt: Pregnancy is an inflammatory process that is carefully regulated by the placenta via immunomodulation and cell-to-cell communication of maternal and fetal tissues. Exosomes, types of extracellular vesicles, facilitate the intercellular communication and traffic biologically modifying cargo within the maternal-placental-fetal axis in normal and pathologic pregnancies. Chorioamnionitis is characterized by inflammation of chorioamniotic membranes that produces systemic maternal and fetal inflammatory responses of cytokine dysregulation and has been associated with brain injury and neurodevelopmental disorders. This review focuses on how pathologic placental exosomes propagate acute and chronic inflammation leading to brain injury. The evidence reviewed here highlights the need to investigate exosomes from pathologic pregnancies and those with known brain injury to identify new diagnostics, biomarkers, and potential therapeutic targets.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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