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Adiponectin induces NF-B activation that leads to suppression of cytokine-induced NF-B activation in vascular endothelial cells: globular adiponectin vs. high molecular weight adiponectin

Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan.

Yoshiyuki Hattori

Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan.

Kikuo Kasai

Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan.

Yasuko Nakano

Department of Medicinal Information, School of Pharmaceutical Sciences, Showa University, Hatanodai, Shinagawa, Tokyo 142-8555, Japan.

Adiponectin circulates in plasma as various isoforms. However, the biological activity of each isoform has not been firmly established. High molecular weight (HMW) adiponectin may be the active form of adiponectin, while a proteolytic cleavage product of adiponectin, known as globular adiponectin (gAd), has recently been shown to activate vascular endothelial cells. We compared HMW adiponectin with gAd to investigate whether they could activate nuclear factor kappa B (NF-B) and suppress cytokine-induced NF-B activation in vascular endothelial cells. HMW adiponectin was found to activate NF-B modestly compared to the activation observed with gAd. HMW adiponectin requires a shorter incubation period to demonstrate inhibition against tumour necrosis factor alpha (TNF)-induced NF-B activation, compared with gAd. gAd strongly activates NF-B, thereby inducing the expression of various pro-inflammatory and adhesion molecule genes, and requires a longer incubation period to show inhibition against cytokine-induced NF-B activation. Thus, HMW adiponectin might function to protect against inflammatory stimuli, while cleavage of adiponectin at inflammatory sites might enhance the inflammatory process.

Key Words: globular adiponectin • high molecular weight adiponectin • NF-B • vascular endothelial cells

Diabetes and Vascular Disease Research, Vol. 5, No. 2, 123-127 (2008)
DOI: 10.3132/dvdr.2008.020


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