title: C1q/TNF-related protein-3 (CTRP-3) attenuates lipopolysaccharide (LPS)-induced systemic inflammation and adipose tissue Erk-1/-2 phosphorylation in mice in vivo.
abstract: BACKGROUND
  The C1q/TNF-related proteins comprise a growing family of adiponectin paralogous proteins. CTRP-3 represents a novel adipokine with strong expression in adipose tissue and was shown to inhibit chemokine and cytokine release in adipocytes and monocytes in vitro. The aim of the study was to gain the proof of principle that CTRP-3 is a potent anti-inflammatory adipokine in vivo.
  
  
  METHODS
  C57BL/6N mice were treated intraperitoneally (i.p.) with bacterial lipopolysaccharide (LPS) for 2h. The effects of a 30 min pre-treatment with CTRP-3 i.p. or intravenously (i.v.) on systemic and on epididymal, perirenal and subcutaneous adipose tissue inflammation was analyzed via real-time RT-PCR, ELISA and Western blot analysis.
  
  
  RESULTS
  LPS (1 μg i.p.) significantly increased serum IL-6 and MIP-2 levels as well as epididymal adipose tissue expression of IL-6 and MIP-2 in mice, whereas CTRP-3 (10 μg i.p.) alone or PBS (i.p.) had no effect. Pre-treatment of mice by CTRP-3 i.p. prior to LPS application significantly attenuated LPS-induced cytokine levels but had no effect on adipose tissue cytokine mRNA expression. In contrast to i.p. application of CTRP-3, systemic i.v. application was not sufficient to inhibit LPS-induced cytokine levels or mRNA tissue expression. CTRP-3 given i.p. significantly attenuated LPS-induced phosphorylation of Erk-1/-2 in inguinal adipose tissue.
  
  
  CONCLUSIONS
  The present study shows the proof of principle that the novel adipokine CTRP-3 is a potent inhibitor of LPS-induced systemic inflammation and LPS-induced signaling in adipose tissue in vivo.
authors.affiliation: Department of Internal Medicine III, Giessen University Hospital, Germany. Electronic address: andreas.schmid@innere.med.uni-giessen.de.
authors.forename: Andreas
authors.initials: A
authors.lastname: Schmid
authors.affiliation: Department of Internal Medicine I, Regensburg University Hospital, Germany.
authors.forename: Andrea
authors.initials: A
authors.lastname: Kopp
authors.affiliation: Department of Internal Medicine I, Regensburg University Hospital, Germany.
authors.forename: Frank
authors.initials: F
authors.lastname: Hanses
authors.affiliation: Department of Internal Medicine III, Giessen University Hospital, Germany.
authors.forename: Thomas
authors.initials: T
authors.lastname: Karrasch
authors.affiliation: Department of Internal Medicine III, Giessen University Hospital, Germany.
authors.forename: Andreas
authors.initials: A
authors.lastname: Schäffler
mesh_terms: D054392:Adipokines / Q000502:physiology*; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010766:Phosphorylation
chemical_list: D054392:Adipokines; C428135:CORS26 protein, mouse; D008070:Lipopolysaccharides
keywords: Adipokine; Adipose tissue; CTRP-3; Erk-1/-2; Inflammation; LPS