To provide insight into the underlying mechanisms for inflammation and remodeling early after TAC we measured RNA or protein levels of candidate cytokine mediators, such as monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), which were known to contribute in other hypertrophy models [10]–[14]. The gene discussed is CCL2; the disease is persistent truncus arteriosus.