Abstract

Clinical and experimental investigations have shown that, during wound healing and fibrocontractive diseases, fibroblasts acquire, more or less permanently according to the situation, morphological and biochemical features of smooth muscle (SM) cells including the expression of alpha-SM actin. Primary and passaged cultures of rat and human fibroblasts contain a subpopulation of cells expressing alpha-SM actin. These cells could derive from SM cells and/or pericytes present in the tissue from which cultures have been produced or represent bona fide fibroblasts. We have investigated the presence of alpha-SM actin in fibroblast cultures, clones, and subclones. In all cases the fibroblastic populations studied showed a proportion of alpha-SM actin expressing cells. Even after cloning, we never obtained populations negative for alpha-SM actin. We conclude that alpha-SM actin expression in fibroblastic cultures is not due to contaminant cells but is a feature of fibroblasts themselves. Our results support the view that fibroblastic cells are a heterogeneous population. It has been previously shown that gamma-interferon (gamma-IFN) decreases alpha-SM actin expression in SM cells. In rat and human fibroblasts, gamma-IFN decreases alpha-SM actin protein and mRNA expression as well as proliferation. The properties of this cytokine make it a good candidate for exerting an anti-fibrotic activity in vivo.