title: Prostacyclin prevents pericyte loss and demyelination induced by lysophosphatidylcholine in the central nervous system.
abstract: Pericytes play pivotal roles in physiological and pathophysiological conditions in the central nervous system. As pericytes prevent vascular leakage, they can halt neuronal damage stemming from a compromised blood-brain barrier. Therefore, pericytes may be a good target for the treatment of neurodegenerative disorders, although evidence is lacking. In this study, we show that prostacyclin attenuates lysophosphatidylcholine (LPC)-mediated vascular dysfunction through pericyte protection in the adult mouse spinal cord. LPC decreased the number of pericytes in an in vitro blood-brain barrier model, and this decrease was prevented by iloprost treatment, a prostacyclin analog. Intrathecal administration of iloprost attenuated vascular barrier disruption after LPC injection in the mouse spinal cord. Furthermore, iloprost treatment diminished demyelination and motor function deficits in mice injected with LPC. These results support the notion that prostacyclin acts on pericytes to maintain vascular barrier integrity.
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, 5 Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan muramatsu@molneu.med.osaka-u.ac.jp.
authors: Rieko
authors: R
authors: Muramatsu
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and.
authors: Mariko
authors: M
authors: Kuroda
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and.
authors: Ken
authors: K
authors: Matoba
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and.
authors: Hsiaoyun
authors: H
authors: Lin
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and.
authors: Chisato
authors: C
authors: Takahashi
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and.
authors: Yoshihisa
authors: Y
authors: Koyama
authors: From the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871 and Core Research for Evolutional Science and Technology and yamashita@molneu.med.osaka-u.ac.jp.
authors: Toshihide
authors: T
authors: Yamashita
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects; D002452:Cell Count; D003711:Demyelinating Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D018450:Disease Progression; D011464:Epoprostenol / Q000378:metabolism*; D005260:Female; D016285:Iloprost / Q000494:pharmacology; D008244:Lysophosphatidylcholines / Q000494:pharmacology*; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D020286:Pericytes / Q000166:cytology* / Q000187:drug effects*; D059748:Proteolysis / Q000187:drug effects; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D013116:Spinal Cord / Q000473:pathology*; D062725:Tight Junction Proteins / Q000378:metabolism
chemical_list: D008244:Lysophosphatidylcholines; D062725:Tight Junction Proteins; D011464:Epoprostenol; D016285:Iloprost
keywords: Axon; Blood-Brain Barrier; Mouse; Multiple Sclerosis; Neurite Outgrowth; Neurodegeneration; Oligodendrocyte; Spinal Cord