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K Ishizawa, Pharmacology, The University of Tokushima Graduate School, Tokushima, 770-8503, Japan
N Dorjsuren, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
Y Izawa-Ishizawa, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
R Sugimoto, Clinical Pharmacy, The University of Tokushima Graduate School, Tokushima, Japan
Y Ikeda, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
Y Kihira, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
K Kawazoe, Clinical Pharmacy, The University of Tokushima Graduate School, Tokushima, Japan
S Tomita, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
K Tsuchiya, Medical Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan
K Minakuchi, Clinical Pharmacy, The University of Tokushima Graduate School, Tokushima, Japan
T Tamaki, Pharmacology, The University of Tokushima Graduate School, Tokushima, Japan

Correspondence: Keisuke Ishizawa, Email: ikeisuke{at}basic.med.tokushima-u.ac.jp

Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function is declined in patient with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathway, in cultured rat mesangial cells (RMCs). PDGF-induced RMC migration was significantly inhibited by pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect on BMK1, p38 MAP kinase and Akt activations in RMC. PDGF-induced BMK1 and p38 MAP kinase activations were significantly attenuated by pretreatment of adiponectin in RMCs. On the other hand, the activation of Akt by PDGF was not diminished by the pretreatment with adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it was implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related with MC disorders.