PMID- 21737957
OWN - NLM
STAT- MEDLINE
DCOM- 20111118
LR  - 20190819
IS  - 1347-4820 (Electronic)
IS  - 1346-9843 (Linking)
VI  - 75
IP  - 8
DP  - 2011
TI  - Effect of adiponectin on cardiac allograft vasculopathy.
PG  - 2005-12
AB  - BACKGROUND: The role of adiponectin (APN), an adipose tissue-specific secretory 
      protein, on chronic rejection after cardiac transplantation in APN-sense 
      transgenic mice (APN-SE) was evaluated. METHODS AND RESULTS: Heterotopic cardiac 
      transplantation in major histocompatibility complex class II-mismatched mice was 
      performed. B6.C-H-2(bm12)KhEg (Bm12) hearts were transplanted into APN-SE, and 
      allografts were harvested at 8 weeks after transplantation. Quantitative 
      polymerase chain reaction (PCR) and immunohistochemical staining showed that the 
      expression of both AdipoR1 and AdipoR2 was induced in APN-SE recipients. 
      Neointimal hyperplasia was significantly decreased in allografts transplanted 
      into APN-SE (luminal occlusion, 8.9 +/- 2.2%) compared to those transplanted into 
      controls (49.4 +/- 10.5%; P=0.011). APN-SE showed significantly reduced mRNA levels 
      of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, IL-6, 
      and monocyte chemoattractant protein-1 (MCP-1) by quantitative PCR. Western blot 
      analysis revealed that the protein levels of IFN-gamma and MCP-1 were reduced in 
      APN-SE recipients. Proliferation of smooth muscle cells stimulated with activated 
      T cells was suppressed by APN addition, and this effect was canceled by treatment 
      with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor. 
      CONCLUSIONS: APN plays a critical role in the attenuation of chronic rejection by 
      suppressing inflammatory cytokine and chemokine expression and enhancing APN 
      receptor expression. APN plays a beneficial role in reducing the progression of 
      cardiac allograft vasculopathy through the AMPK pathway.
FAU - Ishihara, Takashi
AU  - Ishihara T
AD  - Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 
      Tokyo, Japan.
FAU - Haraguchi, Go
AU  - Haraguchi G
FAU - Konishi, Masanori
AU  - Konishi M
FAU - Ohigashi, Hirokazu
AU  - Ohigashi H
FAU - Saito, Kiyomi
AU  - Saito K
FAU - Nakano, Yasuko
AU  - Nakano Y
FAU - Isobe, Mitsuaki
AU  - Isobe M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110706
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Adiponectin)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Receptors, Adiponectin)
RN  - 0 (adiponectin receptor 1, mouse)
RN  - 0 (adiponectin receptor 2, mouse)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/antagonists & inhibitors/genetics/metabolism
MH  - Adiponectin/genetics/*metabolism/pharmacology
MH  - Animals
MH  - Cell Proliferation/drug effects
MH  - Chronic Disease
MH  - Coronary Vessels/*metabolism/pathology
MH  - Graft Rejection/genetics/*metabolism/pathology
MH  - *Heart Transplantation
MH  - Hyperplasia
MH  - Inflammation/genetics/metabolism/pathology
MH  - Lymphocyte Activation/drug effects/genetics
MH  - Mice
MH  - Mice, Transgenic
MH  - Myocytes, Smooth Muscle/metabolism
MH  - Neointima/genetics/*metabolism/pathology
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Receptors, Adiponectin/biosynthesis/genetics
MH  - T-Lymphocytes/metabolism/pathology
MH  - Transplantation, Homologous
EDAT- 2011/07/09 06:00
MHDA- 2011/12/13 00:00
CRDT- 2011/07/09 06:00
PHST- 2011/07/09 06:00 [entrez]
PHST- 2011/07/09 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
AID - JST.JSTAGE/circj/CJ-10-0879 [pii]
AID - 10.1253/circj.cj-10-0879 [doi]
PST - ppublish
SO  - Circ J. 2011;75(8):2005-12. doi: 10.1253/circj.cj-10-0879. Epub 2011 Jul 6.