2013年4月16日
Intercellular signaling pathway among Endothelia, astrocytes and neurons in excitatory neuronal damage.
International journal of molecular sciences
- ,
- 巻
- 14
- 号
- 4
- 開始ページ
- 8345
- 終了ページ
- 57
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.3390/ijms14048345
- 出版者・発行元
- MDPI AG
Neurons interact closely with astrocytes via glutamate; this neuron-glia circuit may play a pivotal role in synaptic transmission. On the other hand, astrocytes contact vascular endothelial cells with their end-feet. It is becoming obvious that non-neuronal cells play a critical role in regulating the neuronal activity in the brain. We find that kainic acid (KA) administration induces the expression of microsomal prostaglandin E synthase-1 (mPGES-1) in venous endothelial cells and the prostaglandin E2 (PGE2) receptor prostaglandin E receptor (EP)-3 on astrocytes. Endothelial mPGES-1 exacerbates KA-induced neuronal damage in in vivo experiments. In in vitro experiments, mPGES-1 produces PGE2, which enhances astrocytic Ca2+ levels via the EP3 receptor and increases Ca2+-dependent glutamate release, thus aggravating neuronal injury. This novel endothelium-astrocyte-neuron signaling pathway may be crucial for driving neuronal damage after repetitive seizures and could be a new therapeutic target for epilepsy and other brain disorders.
- リンク情報
-
- DOI
- https://doi.org/10.3390/ijms14048345
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/23591846
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645746
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000318017100095&DestApp=WOS_CPL
- ID情報
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- DOI : 10.3390/ijms14048345
- ISSN : 1422-0067
- PubMed ID : 23591846
- PubMed Central 記事ID : PMC3645746
- Web of Science ID : WOS:000318017100095