title: Similarity of mouse perivascular and brown adipose tissues and their resistance to diet-induced inflammation.
abstract: Thoracic perivascular adipose tissue (PVAT) is a unique adipose depot that likely influences vascular function and susceptibility to pathogenesis in obesity and the metabolic syndrome. Surprisingly, PVAT has been reported to share characteristics of both brown and white adipose, but a detailed direct comparison to interscapular brown adipose tissue (BAT) has not been performed. Here we show by full genome DNA microarray analysis that global gene expression profiles of PVAT are virtually identical to BAT, with equally high expression of Ucp-1, Cidea, and other genes known to be uniquely or very highly expressed in BAT. PVAT and BAT also displayed nearly identical phenotypes upon immunohistochemical analysis, and electron microscopy confirmed that PVAT contained multilocular lipid droplets and abundant mitochondria. Compared with white adipose tissue (WAT), PVAT and BAT from C57BL6/J mice fed a high-fat diet for 13 wk had markedly lower expression of immune cell-enriched mRNAs, suggesting resistance to obesity-induced inflammation. Indeed, staining of BAT and PVAT for macrophage markers (F4/80 and CD68) in obese mice showed virtually no macrophage infiltration, and FACS analysis of BAT confirmed the presence of very few CD11b(+)/CD11c(+) macrophages in BAT (1.0%) compared with WAT (31%). In summary, murine PVAT from the thoracic aorta is virtually identical to interscapular BAT, is resistant to diet-induced macrophage infiltration, and thus may play an important role in protecting the vascular bed from inflammatory stress.
authors.affiliation: Program in Molecular Medicine, Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
authors.forename: Timothy P
authors.initials: TP
authors.lastname: Fitzgibbons
authors.forename: Sophia
authors.initials: S
authors.lastname: Kogan
authors.forename: Myriam
authors.initials: M
authors.lastname: Aouadi
authors.forename: Greg M
authors.initials: GM
authors.lastname: Hendricks
authors.forename: Juerg
authors.initials: J
authors.lastname: Straubhaar
authors.forename: Michael P
authors.initials: MP
authors.lastname: Czech
mesh_terms: D000273:Adipose Tissue / Q000502:physiology* / Q000648:ultrastructure; D002001:Adipose Tissue, Brown / Q000502:physiology* / Q000648:ultrastructure; D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis; D001808:Blood Vessels / Q000502:physiology* / Q000648:ultrastructure; D004032:Diet / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects; D005434:Flow Cytometry; D007150:Immunohistochemistry; D007249:Inflammation / Q000139:chemically induced* / Q000517:prevention & control*; D007328:Insulin / Q000097:blood; D007473:Ion Channels / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D046228:Microarray Analysis; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000502:physiology; D024101:Mitochondrial Proteins / Q000096:biosynthesis; D020556:Neutrophil Infiltration / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071256:Uncoupling Protein 1
chemical_list: D051017:Apoptosis Regulatory Proteins; C112510:Cidea protein, mouse; D004041:Dietary Fats; D007328:Insulin; D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1