LPA 1/3 overactivation induces neonatal posthemorrhagic hydrocephalus through ependymal loss and ciliary dysfunction-Reference-Cited by-同舟云学术

LPA 1/3 overactivation induces neonatal posthemorrhagic hydrocephalus through ependymal loss and ciliary dysfunction

Published:2019-10-04 Issue:10 Volume:5 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Lummis Nicole C.¹²^ORCID,Sánchez-Pavón Paloma¹³,Kennedy Grace¹,Frantz Aaron J.¹²^ORCID,Kihara Yasuyuki¹^ORCID,Blaho Victoria A.¹^ORCID,Chun Jerold¹^ORCID

Affiliation:

1. Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.

2. Biomedical Sciences Graduate Program, University of California San Diego School of Medicine, La Jolla, CA, USA.

3. Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.

Abstract

LPA, a blood-borne signaling lipid, induces neonatal hydrocephalus by damaging ependymal cells through LPA 1/3 overactivation.

Funder

U.S. Department of Defense

National Institute of Mental Health

National Heart, Lung, and Blood Institute

National Institute of General Medical Sciences

National Institute of Neurological Disorders and Stroke

American Heart Association

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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4. Global hydrocephalus epidemiology and incidence: Systematic review and meta-analysis;Dewan M. C.;J. Neurosurg.,2018

5. LPA receptor signaling: Pharmacology, physiology, and pathophysiology;Yung Y. C.;J. Lipid Res.,2014

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