title: The Double Roles of the Prostaglandin E2 EP2 Receptor in Intracerebral Hemorrhage.
abstract: BACKGROUND
  Intracerebral hemorrhage (ICH), a subtype of stroke, brings high morbidity and mortality to human beings. Multiple studies indicated that neuroinflammation, excitotoxicity, oxidative stress, cytotoxicity resulted from the degradation products of blood clot play vital roles in ICH-induced secondary brain injury, which contributes to deterioration of neurological outcome. Prostaglandin E2 (PGE2), a type of prostanoids commonly up-regulated in these progresses, is proved to modulate numerous cellular and molecular processes by activating EP2 receptor after ICH.
  
  
  OBJECTIVE
  This review aim to discuss the PGE2 biosynthesis, downstream signaling pathway of EP2 receptor and the roles of EP2 receptor in ICH-induced brain damage, targeting to provide a potential effective therapeutic strategy.
  
  
  METHODS
  A large number of literatures on EP2receptors and intracerebral hemorrhage were searched in PubMed, Medline, and Ebase.
  
  
  RESULTS
  Previous studies showed that EP2 receptor mediated double effects in ICH via activation of different signaling pathway. EP2 receptor could induce neuroprotection, spatial learning, and neuroplasticity via cAMP-PKA signaling pathway, while strengthen inflammation mainly through the cAMP-Epac pathway. In addition, the concentration level of cAMP might be the key factor that decides which downstream signaling pathway would be activated.
  
  
  CONCLUSIONS
  In different phase of cerebral hemorrhage, EP2 receptor plays diverse effects in brain damage through different downstream signaling pathways.
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Luo
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Qiquan
authors.initials: Q
authors.lastname: Zhu
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Huang
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Zongyi
authors.initials: Z
authors.lastname: Xie
authors.affiliation: Department of Neurosurgery, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Cheng
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000209:etiology / Q000378:metabolism*; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis*; D006801:Humans; D018078:Receptors, Prostaglandin E / Q000378:metabolism*; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D018078:Receptors, Prostaglandin E; D017868:Cyclic AMP-Dependent Protein Kinases; D015232:Dinoprostone
keywords: EP2 receptor; ICH-induced brain injury; Intracerebral hemorrhage; prostaglandin E2