|  Help  |  About  |  Contact Us

Publication : Endothelial Microsomal Prostaglandin E Synthetase-1 Upregulates Vascularity and Endothelial Interleukin-1β in Deteriorative Progression of Experimental Autoimmune Encephalomyelitis.

First Author  Takemiya T Year  2018
Journal  Int J Mol Sci Volume  19
Issue  11 PubMed ID  30463256
Mgi Jnum  J:295495 Mgi Id  MGI:6453882
Doi  10.3390/ijms19113647 Citation  Takemiya T, et al. (2018) Endothelial Microsomal Prostaglandin E Synthetase-1 Upregulates Vascularity and Endothelial Interleukin-1beta in Deteriorative Progression of Experimental Autoimmune Encephalomyelitis. Int J Mol Sci 19(11):3647
abstractText  Microsomal prostaglandin E synthetase-1 (mPGES-1) is an inducible terminal enzyme for the production of prostaglandin E(2) (PGE(2)). In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, mPGES-1 is induced in vascular endothelial cells (VECs) around inflammatory foci and facilitates inflammation, demyelination, and paralysis. Therefore, we investigated the role of CD31-positive VECs in mPGES-1-mediated EAE aggravation using immunohistochemical analysis and imaging of wild-type (wt) and mPGES-1-deficient (mPGES-1(-/-)) mice. We demonstrated that EAE induction facilitated vascularity in inflammatory lesions in the spinal cord, and this was significantly higher in wt mice than in mPGES-1(-/-) mice. In addition, endothelial interleukin-1beta (IL-1beta) production was significantly higher in wt mice than in mPGES-1(-/-) mice. Moreover, endothelial PGE(2) receptors (E-prostanoid (EP) receptors EP1(-)4) were expressed after EAE induction, and IL-1beta was induced in EP receptor-positive VECs. Furthermore, IL-1 receptor 1 expression on VECs was increased upon EAE induction. Thus, increased vascularity is one mechanism involved in EAE aggravation induced by mPGES-1. Furthermore, mPGES-1 facilitated the autocrine function of VECs upon EP receptor induction and IL-1beta production, modulating mPGES-1 induction in EAE.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Bio Entities

Trail: Publication

0 Expression