Document Detail


Angiogenesis induced by CNS inflammation promotes neuronal remodeling through vessel-derived prostacyclin.
MedLine Citation:
PMID:  23042236     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Angiogenesis is a prominent feature of central nervous system (CNS) disease and has roles in both the continued promotion of inflammation and the subsequent repair processes. Here we report that prostacyclin (or prostaglandin I(2) (PGI(2))) derived from new vessels promotes axonal remodeling of injured neuronal networks after CNS inflammation. In a localized model of experimental autoimmune encephalomyelitis (EAE), new vessels formed around the inflammatory lesion, followed by sprouting of adjacent corticospinal tract (CST) fibers. These sprouting fibers formed a compensatory motor circuit, leading to recovery of motor function. Capillary endothelial cell-derived prostacyclin bound to its receptor, the type I prostaglandin receptor (IP receptor), on CST neurons, promoting sprouting of CST fibers and contributing to the repair process. Inhibition of prostacyclin receptor signaling impaired motor recovery, whereas the IP receptor agonist iloprost promoted axonal remodeling and motor recovery after the induction of EAE. These findings reveal an important function of angiogenesis in neuronal rewiring and suggest that prostacyclin is a promising molecule for enhancing functional recovery from CNS disease.
Authors:
Rieko Muramatsu; Chisato Takahashi; Shuzo Miyake; Harutoshi Fujimura; Hideki Mochizuki; Toshihide Yamashita
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-10-07
Journal Detail:
Title:  Nature medicine     Volume:  -     ISSN:  1546-170X     ISO Abbreviation:  Nat. Med.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-8     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9502015     Medline TA:  Nat Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
1] Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. [2] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Tokyo, Japan.
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