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High molecular weight adiponectin activates AMPK and suppresses cytokine‐induced NF‐κB activation in vascular endothelial cells
Author(s) -
Hattori Yoshiyuki,
Nakano Yasuko,
Hattori Sachiko,
Tomizawa Atsuko,
Inukai Kouichi,
Kasai Kiuo
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.04.037
Subject(s) - adiponectin , ampk , enos , chemistry , proinflammatory cytokine , medicine , endocrinology , nf κb , protein kinase a , phosphorylation , amp activated protein kinase , cytokine , microbiology and biotechnology , signal transduction , inflammation , biology , biochemistry , nitric oxide , nitric oxide synthase , insulin resistance , insulin
Various isoforms of adiponectin circulate in the plasma. We purified high molecular weight (HMW) adiponectin from human plasma. HMW adiponectin was observed to activate AMP‐activated protein kinase (AMPK), thereby increasing the phosphorylation of eNOS and NO production in endothelial cells. On the other hand, cells preincubated with HMW adiponectin had reduced TNFα‐induced NF‐κB activation. HMW adiponectin by itself was found to modestly activate NF‐κB, which was significantly enhanced by inhibition of AMPK/eNOS activation. Thus, HMW adiponectin might have dual action, both pro and anti‐inflammatory. An initial period of NF‐κB activation by HMW adiponectin might be proinflammatory, but it could be counteracted by activation of AMPK/eNOS, which lead to a potential reduction in a second activation of NF‐κB against inflammatory stimuli.