Abstract 15660: Tissue Remodeling and Pulmonary Fibrosis Development in Chronic Heart Failure
Over 5 million people suffer from heart failure (HF) in the USA (1). Chronic HF leads to irreversible changes in the lung architecture including tissue remodeling and the development of pulmonary fibrosis. Preliminary data from our rat model show that left-sided HF induces pulmonary edema triggering fibroblast remodeling and fibrosis development. Our hypothesis is that fibroblasts undergo phenotypic changes with chronic exposure to cytokines secreted by neutrophils and/or macrophages in chronic HF. We utilized our chronic HF rat model and primary cell cultures to determine phenotypic changes related to fibrosis development in pulmonary fibroblasts. Lung fibroblasts isolated from rat lung after 7 days of HF were significantly more proliferative compared to cells isolated from control lungs (Fig 1 [n=3/group; p<0.5 vs. control]). Collagen production in lung fibroblasts isolated from the HF group doubled compared to collagen production in control lung fibroblasts (Fig 2 [n=3/group; p<0.5 vs. control]). Lung fibroblasts from the HF group also expressed more smooth muscle actin indicating differentiation to a more myofibroblast phenotype (Fig 3 [n=3/group; p<0.5 vs. control]). In summary, our data are essential to facilitate the identification of drug targets and treatment strategies to improve outcomes in HF patients. 1. Lloyd-Jones D et al. Circulation 121:948-54, 2010.
- © 2011 by American Heart Association, Inc.