LPA
Animals
Animals, Newborn
Apoptosis
Brain
/ metabolism
Calcium-Binding Proteins
/ metabolism
Disease Models, Animal
Ependyma
/ cytology
Ependymoglial Cells
/ cytology
Infant, Premature, Diseases
/ chemically induced
Isoxazoles
/ pharmacology
Lysophospholipids
/ toxicity
Macrophages
/ cytology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Microfilament Proteins
/ metabolism
Phagocytosis
Propionates
/ pharmacology
Receptors, Lysophosphatidic Acid
/ antagonists & inhibitors
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
01
03
2019
accepted:
14
09
2019
entrez:
22
10
2019
pubmed:
22
10
2019
medline:
20
5
2020
Statut:
epublish
Résumé
Posthemorrhagic hydrocephalus (PHH) in premature infants is a common neurological disorder treated with invasive neurosurgical interventions. Patients with PHH lack effective therapeutic interventions and suffer chronic comorbidities. Here, we report a murine lysophosphatidic acid (LPA)-induced postnatal PHH model that maps neurodevelopmentally to premature infants, a clinically accessible high-risk population, and demonstrates ventriculomegaly with increased intracranial pressure. Administration of LPA, a blood-borne signaling lipid, acutely disrupted the ependymal cells that generate CSF flow, which was followed by cell death, phagocytosis, and ventricular surface denudation. This mechanism is distinct from a previously reported fetal model that induces PHH through developmental alterations. Analyses of LPA receptor-null mice identified LPA
Identifiants
pubmed: 31633020
doi: 10.1126/sciadv.aax2011
pii: aax2011
pmc: PMC6785248
doi:
Substances chimiques
3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid
0
Aif1 protein, mouse
0
Calcium-Binding Proteins
0
Isoxazoles
0
Lysophospholipids
0
Microfilament Proteins
0
Propionates
0
Receptors, Lysophosphatidic Acid
0
lysophosphatidic acid
PG6M3969SG
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
eaax2011Subventions
Organisme : NINDS NIH HHS
ID : R01 NS084398
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH051699
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007752
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS103940
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141880
Pays : United States
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).
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