title: The novel adipokine C1q/TNF-related protein-3 is expressed in human adipocytes and regulated by metabolic and infection-related parameters.
abstract: BACKGROUND
  The growing family of C1Q/TNF-related proteins is characterized by structural homologies to the anti-inflammatory adipokine adiponectin. CTRP-3 was recently reported to function as an anti-inflammatory LPS-antagonist in vitro.
  
  
  METHODS
  Human subcutaneous and visceral adipocytes and murine 3T3-L1 adipocytes were used for analysis of CTRP-3 expression and function. Western blot analysis of CTRP-3, siRNA mediated knockdown of CTRP-3, Oil red O staining, assessment of basal and epinephrine-induced lipolysis, ELISA-based measurements of supernatant chemokines, recombinant CTRP-3 protein expression, and Staphylococcus aureus (S. aureus) infection assays were used.
  
  
  RESULTS
  CTRP-3 is expressed in subcutaneous and visceral adipocytes. CTRP-3 is positively regulated by insulin, whereas chronic LPS-exposure inhibits terminal adipocyte differentiation and CTRP-3 expression. Intracellular infection of adipocytes by S. aureus also decreases CTRP-3 expression. As demonstrated by siRNA-mediated cellular knockdown of CTRP-3 in adipocytes, CTRP-3 regulates resistin secretion and lipolysis.
  
  
  CONCLUSIONS
  CTRP-3 is expressed in human adipocytes and plays an important role in adipocyte physiology such as lipolysis and adipokine secretion. Both, metabolic factors and infection/inflammation-related factors regulate CTRP-3 expression.
authors.affiliation: Department of Internal Medicine I, Regensburg University Hospital, Regensburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Schmid
authors.forename: A
authors.initials: A
authors.lastname: Kopp
authors.forename: F
authors.initials: F
authors.lastname: Hanses
authors.forename: M
authors.initials: M
authors.lastname: Bala
authors.forename: M
authors.initials: M
authors.lastname: Müller
authors.forename: A
authors.initials: A
authors.lastname: Schäffler
mesh_terms: D041721:3T3-L1 Cells; D054392:Adipokines / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D004837:Epinephrine / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D020868:Gene Silencing; D006801:Humans; D007328:Insulin / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008066:Lipolysis; D051379:Mice; D011994:Recombinant Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D052243:Resistin / Q000378:metabolism; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology; D013211:Staphylococcus aureus / Q000276:immunology; D050151:Subcutaneous Fat / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D054392:Adipokines; C506069:C1QTNF3 protein, human; C428135:CORS26 protein, mouse; D007328:Insulin; D011994:Recombinant Proteins; D052243:Resistin; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors; D004837:Epinephrine