Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling
Joint Authors
Moon, Eunjung
Han, Jeong Eun
Jeon, Sejin
Ryu, Jong Hoon
Choi, Ji Woong
Chun, Jerold
Source
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-10-20
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Initial and recurrent stroke produces central nervous system (CNS) damage, involving neuroinflammation.
Receptor-mediated S1P signaling can influence neuroinflammation and has been implicated in cerebral ischemia through effects on the immune system.
However, S1P-mediated events also occur within the brain itself where its roles during stroke have been less well studied.
Here we investigated the involvement of S1P signaling in initial and recurrent stroke by using a transient middle cerebral artery occlusion/reperfusion (M/R) model combined with analyses of S1P signaling.
Gene expression for S1P receptors and involved enzymes was altered during M/R, supporting changes in S1P signaling.
Direct S1P microinjection into the normal CNS induced neuroglial activation, implicating S1P-initiated neuroinflammatory responses that resembled CNS changes seen during initial M/R challenge.
Moreover, S1P microinjection combined with M/R potentiated brain damage, approximating a model for recurrent stroke dependent on S1P and suggesting that reduction in S1P signaling could ameliorate stroke damage.
Delivery of FTY720 that removes S1P signaling with chronic exposure reduced damage in both initial and S1P-potentiated M/R-challenged brain, while reducing stroke markers like TNF-α.
These results implicate direct S1P CNS signaling in the etiology of initial and recurrent stroke that can be therapeutically accessed by S1P modulators acting within the brain.
American Psychological Association (APA)
Moon, Eunjung& Han, Jeong Eun& Jeon, Sejin& Ryu, Jong Hoon& Choi, Ji Woong& Chun, Jerold. 2015. Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling. Mediators of Inflammation،Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072383
Modern Language Association (MLA)
Moon, Eunjung…[et al.]. Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling. Mediators of Inflammation No. 2015 (2015), pp.1-12.
https://search.emarefa.net/detail/BIM-1072383
American Medical Association (AMA)
Moon, Eunjung& Han, Jeong Eun& Jeon, Sejin& Ryu, Jong Hoon& Choi, Ji Woong& Chun, Jerold. Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling. Mediators of Inflammation. 2015. Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072383
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1072383