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

Autor: Marumi Kawakami, Chisen Takeuchi, Takako Takemiya
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
vascular endothelial cells
interleukin-1β
medicine.medical_treatment
Interleukin-1beta
experimental autoimmune encephalomyelitis
multiple sclerosis
lcsh:Chemistry
0302 clinical medicine
Prostaglandin E2
Receptor
lcsh:QH301-705.5
Spectroscopy
Prostaglandin-E Synthases
Chemistry
Experimental autoimmune encephalomyelitis
General Medicine
Up-Regulation
Computer Science Applications
Platelet Endothelial Cell Adhesion Molecule-1
Spinal Cord
Disease Progression
microsomal prostaglandin E synthetase-1
Immunohistochemistry
Female
lipids (amino acids
peptides
and proteins)
medicine.symptom
Prostaglandin E
medicine.drug
musculoskeletal diseases
medicine.medical_specialty
Encephalomyelitis
Autoimmune
Experimental
Inflammation
Models
Biological
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
Microsomes
Internal medicine
medicine
Animals
Paralysis
Receptors
Prostaglandin E
Physical and Theoretical Chemistry
Autocrine signalling
Molecular Biology
prostaglandin E2
Multiple sclerosis
Organic Chemistry
Endothelial Cells
Receptors
Interleukin-1
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Endocrinology
lcsh:Biology (General)
lcsh:QD1-999
030217 neurology & neurosurgery
Demyelinating Diseases
Zdroj: International Journal of Molecular Sciences, Vol 19, Iss 11, p 3647 (2018)
International Journal of Molecular Sciences
Volume 19
Issue 11
ISSN: 1422-0067
Popis: Microsomal prostaglandin E synthetase-1 (mPGES-1) is an inducible terminal enzyme for the production of prostaglandin E2 (PGE2). 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&minus
/&minus
) 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&minus
mice. In addition, endothelial interleukin-1&beta
(IL-1&beta
) production was significantly higher in wt mice than in mPGES-1&minus
mice. Moreover, endothelial PGE2 receptors (E-prostanoid (EP) receptors EP1&ndash
4) were expressed after EAE induction, and IL-1&beta
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-1&beta
production, modulating mPGES-1 induction in EAE.
Databáze: OpenAIRE
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