title: Adiponectin accumulates in myocardial tissue that has been damaged by ischemia-reperfusion injury via leakage from the vascular compartment.
abstract: OBJECTIVE
  Adiponectin, a circulating adipocyte-derived hormone, exerts beneficial actions on hearts subjected to ischemia-reperfusion injury. Adiponectin exists in plasma as three different oligomeric forms: trimer, hexamer and high molecular weight. This study investigated the expression and myocardial accumulation of adiponectin in a murine model of ischemia-reperfusion injury.
  
  
  METHODS
  Wild-type and adiponectin deficient mice were subjected to left anterior descending artery ligation followed by reperfusion. Plasma adiponectin levels were analyzed by ELISA and adiponectin in heart was determined by immunohistochemical, Western blot and real-time PCR analyses.
  
  
  RESULTS
  Plasma adiponectin levels declined after myocardial ischemia-reperfusion injury due to reductions in high molecular weight and, to a lesser extent, trimer and hexamer isoforms. Adiponectin protein was detected in injured but not sham-operated heart, and this was accompanied by a negligible increase in adiponectin transcript in the myocardium. Systemic delivery of adiponectin to adiponectin knockout (APN-KO) mice led to the accumulation of adiponectin in ischemia-reperfusion-injured, but not-uninjured hearts at levels comparable to wild-type suggesting that cardiac expression of adiponectin does not appreciably contribute to its accumulation in the infarcted heart. The serum half-life of adiponectin was 7.4+/-0.3 h in ischemia-reperfusion and 9.7+/-0.5 h in sham-operated mice (P>0.05), whereas the half-life of adiponectin in the damaged heart was 26.9+/-2.2 h (P<0.05).
  
  
  CONCLUSIONS
  These data show that adiponectin accumulates in the heart following ischemic damage primarily through leakage from the vascular compartment, and that adiponectin has a longer half-life in damaged heart tissue than in plasma.
authors.affiliation: Molecular Cardiology/Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA.
authors.forename: Rei
authors.initials: R
authors.lastname: Shibata
authors.forename: Kaori
authors.initials: K
authors.lastname: Sato
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kumada
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Izumiya
authors.forename: Mina
authors.initials: M
authors.lastname: Sonoda
authors.forename: Shinji
authors.initials: S
authors.lastname: Kihara
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Ouchi
authors.forename: Kenneth
authors.initials: K
authors.lastname: Walsh
mesh_terms: D052242:Adiponectin / Q000032:analysis* / Q000097:blood / Q000235:genetics; D000818:Animals; D001808:Blood Vessels / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D015151:Immunoblotting; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D052242:Adiponectin; D012333:RNA, Messenger