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Distribution of microsomal prostaglandin E synthase‐1 in the mouse brain
Author(s) -
Eskilsson Anna,
Tachikawa Masanori,
Hosoya Kenichi,
Blomqvist Anders
Publication year - 2014
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.23593
Subject(s) - circumventricular organs , biology , subfornical organ , area postrema , choroid plexus , endocrinology , medicine , inflammation , cyclooxygenase , immune system , stimulation , microglia , prostaglandin , central nervous system , microbiology and biotechnology , immunology , biochemistry , angiotensin ii , blood pressure , enzyme
Previous studies in rats have demonstrated that microsomal prostaglandin E synthase‐1 (mPGES‐1) is induced in brain vascular cells that also express inducible cyclooxygenase‐2, suggesting that such cells are the source of the increased PGE 2 levels that are seen in the brain following peripheral immune stimulation, and that are associated with sickness responses such as fever, anorexia, and stress hormone release. However, while most of what is known about the functional role of mPGES‐1 for these centrally evoked symptoms is based on studies on genetically modified mice, the cellular localization of mPGES‐1 in the mouse brain has not been thoroughly determined. Here, using a newly developed antibody that specifically recognizes mouse mPGES‐1 and dual‐labeling for cell‐specific markers, we report that mPGES‐1 is constitutively expressed in the mouse brain, being present not only in brain endothelial cells, but also in several other cell types and structures, such as capillary‐associated pericytes, astroglial cells, leptomeninges, and the choroid plexus. Regional differences were seen with particularly prominent labeling in autonomic relay structures such as the area postrema, the subfornical organ, the paraventricular hypothalamic nucleus, the arcuate nucleus, and the preoptic area. Following immune stimulation, mPGES‐1 in brain endothelial cells, but not in other mPGES‐1‐positive cells, was coexpressed with cyclooxygenase‐2, whereas there was no coexpression between mPGES‐1 and cyclooxygenase‐1. These data imply a widespread synthesis of PGE 2 or other mPGES‐1‐dependent products in the mouse brain that may be related to inflammation‐induced sickness symptom as well as other functions, such as blood flow regulation. J. Comp. Neurol. 522:3229–3244, 2014. © 2014 Wiley Periodicals, Inc.