Serum collected from rats with myocardial infarction increases extracellular matrix accumulation by myofibroblasts isolated from myocardial infarction scar

Abstract

The effect on extracellular matrix content is believed to be an average of several serum derived compounds acting in opposition. The aim of the study is to determine whether whole serum of rats with myocardial infarction may modify the accumulation of extracellular matrix in cultures of myofibroblasts isolated from the myocardial infarction scar. A second aim is to determine whether the tested serum can also degranulate the mast cells. Serum was collected from rats with sham myocardial infarction, rats with myocardial infarction induced by coronary artery ligation and control animals. The experiments were carried out on myocardial infarction scar myofibroblasts or mast cells from the peritoneal cavity. The cultures were divided into three groups containing eight cultures each: one treated with serum from control rats, from animals after sham operation or from those after myocardial infarction. In all groups, the serum was used at concentrations of 10%, 20% or 30%. The total collagen content (Woesner method) glycosaminoglycan level (Farandale method), cell proliferation (BrdU), histamine secretion from mast cells (spectrofluorymetry), β1 integrin and α-smooth muscle actin expression (flow cytometry) were evaluated. Isolated cells were α-smooth muscle actin positive and identified as myofibroblasts. Serum derived from rats with myocardial infarction increased collagen and glycosaminoglycan content in the cultures and modified myofibroblast proliferation in a concentration-dependent manner. The serum also results in an imbalance between collagen and glycosaminoglycan levels. The content of β1 integrin was not influenced by myocardial infarction serum. The serum of rats with myocardial infarction is involved in regulation of collagen and glycosaminoglycan content in myofibroblast cultures, as well as the modification of their proliferation. These changes were not accompanied with integrin β1 density variations. The serum of the myocardial infarction rats did not influence the mast cell degranulation.