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Potential anti-inflammatory role of activin A in acute coronary syndromes

Camilla Smith, MD^*, Arne Yndestad, MSc^*, Bente Halvorsen, MSc, PhD^*, Thor Ueland, BS^*, Torgun Wæhre, MD^*, Kari Otterdal, MSc^*, Hanne Scholz, MSc^*, Knut Endresen, MD, PhD, Lars Gullestad, MD, PhD^||, Stig S. Frøland, MD, PhD^*, Jan Kristian Damås, MD, PhD^* and Pål Aukrust, MD, PhD^*,*

^* Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
Department of Cardiology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
Section of Endocrinology, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway
^|| Department of Medicine, Bærum Hospital, Sandvika, Norway

View larger version (32K): [in a new window]   Figure 1 (A) Serum levels of activin A and (B) plasma levels of follistatin in 20 patients with unstable angina pectoris (AP), 26 patients with stable AP, and 20 healthy controls. Data are presented as the mean value ± SEM. *p < 0.05 and **p < 0.01 versus healthy controls.

View larger version (29K): [in a new window]   Figure 2 Gene expression of the activin A subunit activin betaA (A) and the activin A receptor II type A (ARIIA) (B) and type B (ARIIB) (C) in peripheral blood mononuclear cells from 15 patients with unstable angina pectoris (AP), 15 patients with stable AP, and 10 healthy controls. The messenger ribonucleic acid (mRNA) levels were quantified using real-time reverse transcription polymerase chain reaction, and data are presented relative to the gene expression of beta-actin (mean ± SEM). *p < 0.05 versus healthy controls. p < 0.05 versus stable AP.

View larger version (26K): [in a new window]   Figure 3 Gene expression of Smad2 (A), Smad3 (B), and Smad7 (C) in peripheral blood mononuclear cells from 15 patients with unstable angina pectoris (AP), 15 patients with stable AP, and 10 healthy controls. The messenger ribonucleic acid (mRNA) levels were quantified using real-time quantitative reverse transcription polymerase chain reaction, and data are presented relative to the gene expression of beta-actin (mean ± SEM). *p < 0.05 versus healthy controls. p < 0.05 versus stable AP.

View larger version (36K): [in a new window]   Figure 4 Plasma levels of activin A and follistatin in 14 patients with stable angina pectoris (AP) (A and C) and 13 patients with unstable AP (B and D) before (Pre) and 48 h after (Post) percutaneous coronary intervention (PCI). Activin A levels were only measured in 11 of the patients with unstable AP.

View larger version (29K): [in a new window]   Figure 5 The effect of activin A (10 and 100 ng/ml) on the protein levels of interleukin (IL)-6 (A), IL-8 (B), macrophage inflammatory protein (MIP)-1-alpha (C), and tumor necrosis alpha (TNF)-alpha (D) in peripheral blood mononuclear cells supernatants from six patients with unstable angina pectoris (AP) (solid bars), seven patients with stable AP (striped bars), and six healthy controls (open bars) after culturing for 18 h. Data are given as the mean value ± SEM. *p < 0.05 versus unstimulated cells.