Abstract:
: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 LPA1 and LPA3 as key mediators of PHH. Pharmacological blockade of LPA1 prevented PHH in LPA-injected animals, supporting the medical tractability of LPA receptor antagonists in preventing PHH and negative CNS sequelae in premature infants.
journal_name
Sci Advjournal_title
Science advancesauthors
Lummis NC,Sánchez-Pavón P,Kennedy G,Frantz AJ,Kihara Y,Blaho VA,Chun Jdoi
10.1126/sciadv.aax2011subject
Has Abstractpub_date
2019-10-09 00:00:00pages
eaax2011issue
10issn
2375-2548pii
aax2011journal_volume
5pub_type
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