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Globular Adiponectin Activates Nuclear Factor-B and Activating Protein-1 and Enhances Angiotensin II–Induced Proliferation in Cardiac Fibroblasts

¹ Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi, Japan
² Laboratory of Molecular and Cellular Biology, Dokkyo University School of Medicine, Mibu, Tochigi, Japan
³ Department of Hypertension and Cardiorenal Medicine, Dokkyo University School of Medicine, Mibu, Tochigi, Japan

Address correspondence and reprint requests to Yoshiyuki Hattori, MD, Department of Endocrinology and Metabolism, Dokkyo Medical University School of Medicine, Mibu, Tochigi 321-0293, Japan. E-mail yhattori{at}dokkyomed.ac.jp

Abbreviations: AdipoR, adiponectin receptor; Ang II, angiotensin II; AP-1, activating protein-1; C1qR, C1q receptor; ERK, extracellular signal–regulated kinase; gAd, globular adiponectin; IL, interleukin; NF-B, nuclear factor-B; siRNA, small interference RNA; TNF-, tumor necrosis factor-

Adiponectin is present in the serum as a trimer, hexamer, or high–molecular weight form. A proteolytic cleavage product of adiponectin, known as globular adiponectin (gAd), also circulates in human plasma. The biological activities of these isoforms are not well characterized. Pressure overload in adiponectin-deficient mice results in enhanced concentric cardiac hypertrophy and increased mortality, suggesting that adiponectin inhibits hypertrophic signaling in the myocardium. Therefore, we examined whether gAd exerts the same effects on myocardium signaling. Nuclear factor-B (NF-B) and activating protein-1 (AP-1) activation were examined using cardiac fibroblasts prepared from the ventricles of 1- to 2-day-old Wistar rats and grown in culture. gAd activated NF-B and enhanced tumor necrosis factor- (TNF-)-induced NF-B activity. gAd also activated AP-1 and enhanced angiotensin II (Ang II)-induced AP-1 activity. gAd induced mRNA expression of c-fos and c-jun and activated extracellular signal–regulated kinase. Thus, gAd enhanced Ang II–induced DNA and collagen synthesis. Antibodies against adiponectin receptor (AdipoR)1 and AdipoR2 elicit activation of NF-B or AP-1, two redox-sensitive transcription factors. Thus, rather than having an antihypertrophic effect, gAd might contribute to the activation of myocardium signaling, leading to myocardial hypertrophy.

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This article has been cited by other articles:

				B. J. Goldstein, R. Scalia, X. L. Ma, K. Mahadev, X. Wu, and R. Ouedraogo Comment on: Hattori et al. (2007) Globular Adiponectin Activates Nuclear Factor-{kappa}B and Activating Protein-1 and Enhances Angiotensin II-Induced Proliferation in Cardiac Fibroblasts: Diabetes 56:804-808 Diabetes, July 1, 2007; 56(7): e7 - e8. [Full Text] [PDF]

				Y. Hattori and Y. Nakano Response to Comment on: Goldstein et al. (2007) Globular Adiponectin Activates Nuclear Factor-{kappa}B and Activating Protein-1 and Enhances Angiotensin II-Induced Proliferation in Cardiac Fibroblasts: Diabetes 56:804-808 Diabetes, July 1, 2007; 56(7): e9 - e10. [Full Text] [PDF]