Lysophosphatidylcholine induces glial cell activation: Role of rho kinase
Identifieur interne : 001F81 ( Main/Exploration ); précédent : 001F80; suivant : 001F82Lysophosphatidylcholine induces glial cell activation: Role of rho kinase
Auteurs : Abdullah Md. Sheikh [Japon] ; Atsushi Nagai [Japon] ; Jae K. Ryu [Canada] ; James G. Mclarnon [Canada] ; Seung U. Kim [Canada] ; Junichi Masuda [Japon]Source :
- Glia [ 0894-1491 ] ; 2009-06.
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Abstract
Lysophosphatidylcholine (LPC), a major phospholipid component of atherogenic oxidized LDL, is implicated in atherosclerosis and, recently, in neurodegenerative diseases. We investigated the immunomodulatory functions of LPC in the central nervous system (CNS) using both an in vivo rat model, and in vitro culture systems of human primary astrocytes and a microglia cell line, HMO6. Compared with PBS injection, 20 nmol LPC‐injection into the rat striatum increased astrocyte and microglial accumulation and elevated iNOS expression; concomitantly a time‐dependent decrease in number of neurons was exhibited. In vitro studies on astrocytes and HMO6 cells showed that LPC increased the gene expression of proinflammatory factors IL‐1β, COX‐2, and GM‐CSF. LPC also induced chemotactic responses in HMO6 cells. Inhibition of rho kinase by fasudil, Y27632, or expressing a dominant negative form of rho kinase inhibited the LPC‐induced IL‐1β mRNA expression in both astrocytes and HMO6. Moreover, intraperitoneal fasudil injection inhibited the LPC‐induced microglial accumulation and iNOS expression and also was effective in protecting against neuronal loss. Silencing G2A, a specific receptor for LPC, inhibited proinflammatory gene expression and HMO6 migration. Overall, our results indicate that LPC induced considerable neuroinflammatory reactivity in glia mediated by rho kinase‐dependent pathways with inhibition of these pathways conferring significant extents of neuroprotection. © 2008 Wiley‐Liss, Inc.
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DOI: 10.1002/glia.20815
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Sheikh</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory Medicine, Shimane University School of Medicine, 89‐1 Enya cho, Izumo 693‐8501</wicri:regionArea><wicri:noRegion>Izumo 693‐8501</wicri:noRegion></affiliation></author><author><name sortKey="Nagai, Atsushi" sort="Nagai, Atsushi" uniqKey="Nagai A" first="Atsushi" last="Nagai">Atsushi Nagai</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory Medicine, Shimane University School of Medicine, 89‐1 Enya cho, Izumo 693‐8501</wicri:regionArea><wicri:noRegion>Izumo 693‐8501</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Laboratory Medicine, Faculty of Medicine, Shimane University, 89‐1 Enya cho, Izumo 693‐8501</wicri:regionArea><wicri:noRegion>Izumo 693‐8501</wicri:noRegion></affiliation></author><author><name sortKey="Ryu, Jae K" sort="Ryu, Jae K" uniqKey="Ryu J" first="Jae K." last="Ryu">Jae K. 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We investigated the immunomodulatory functions of LPC in the central nervous system (CNS) using both an in vivo rat model, and in vitro culture systems of human primary astrocytes and a microglia cell line, HMO6. Compared with PBS injection, 20 nmol LPC‐injection into the rat striatum increased astrocyte and microglial accumulation and elevated iNOS expression; concomitantly a time‐dependent decrease in number of neurons was exhibited. In vitro studies on astrocytes and HMO6 cells showed that LPC increased the gene expression of proinflammatory factors IL‐1β, COX‐2, and GM‐CSF. LPC also induced chemotactic responses in HMO6 cells. Inhibition of rho kinase by fasudil, Y27632, or expressing a dominant negative form of rho kinase inhibited the LPC‐induced IL‐1β mRNA expression in both astrocytes and HMO6. Moreover, intraperitoneal fasudil injection inhibited the LPC‐induced microglial accumulation and iNOS expression and also was effective in protecting against neuronal loss. Silencing G2A, a specific receptor for LPC, inhibited proinflammatory gene expression and HMO6 migration. Overall, our results indicate that LPC induced considerable neuroinflammatory reactivity in glia mediated by rho kinase‐dependent pathways with inhibition of these pathways conferring significant extents of neuroprotection. © 2008 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Canada</li><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Sheikh, Abdullah Md" sort="Sheikh, Abdullah Md" uniqKey="Sheikh A" first="Abdullah Md." last="Sheikh">Abdullah Md. 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