Comment on: Hattori et al. (2007) Globular Adiponectin Activates Nuclear Factor-κB and Activating Protein-1 and Enhances Angiotensin II–Induced Proliferation in Cardiac Fibroblasts: Diabetes 56:804–808
- Barry J. Goldstein1,
- Rosario Scalia2,
- Xin L. Ma3,
- Kalyankar Mahadev1,
- Xiangdong Wu1 and
- Raogo Ouedraogo1
- 1Division of Endocrinology, Diabetes and Metabolic Diseases, Department of Medicine, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania
- 2Department of Molecular Physiology and Biophysics, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania
- 3Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania
- Address correspondence to Barry J. Goldstein, MD, PhD, Division of Endocrinology, Diabetes and Metabolic Diseases, Department of Medicine, Jefferson Medical College, Suite 349, 1020 Locust St., Philadelphia, PA 19107. E-mail: barry.goldstein{at}jefferson.edu
We read with interest the recent articles by Hattori et al. (1,2), which report activation of nuclear factor-κB (NF-κB) transcription by the recombinant globular domain of adiponectin. However, these findings contrast directly with a substantial body of published and ongoing work. As initially reported by Ouchi et al. and confirmed by other groups (3,4), a major effect of adiponectin is the suppression of proinflammatory endothelial responses, which include reversing the activation of NF-κB, reducing adhesion molecule expression, and enhancing nitric oxide bioavailability. We have shown that the globular domain of adiponectin also suppresses endothelial reactive oxygen species generation in response to various agonists, including oxidized LDL and high glucose (5,6). At the American Diabetes Association 66th …
