THE EFFECTS OF CIGARETTE SMOKE ON ADULT MOUSE LUNG PROGENITOR CELL DIFFERENTIATION
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Tobacco smoke promotes a progressive loss of alveolar epithelial cells leading to an increased incidence of lung diseases. One of these diseases, known as Idiopathic Pulmonary Fibrosis (IPF), involves an increase in (myo)fibroblastic cell activity that, in turn, causes the buildup of extracellular matrix and scarring of the lung. Due to their role in the maintenance of healthy tissue, it has been suggested that improperly functioning myofibroblastic stem/progenitor cells play a role in the pathogenesis of IPF. This study attempts to garner insights into the role played by cigarette smoke on the cellular mechanisms that may lead to the development of IPF. We used a novel model that isolates lung progenitor cells from the lungs of mice and follows their growth in vitro. These progenitor cells, known as anchorage-independent cells (AICs), have been shown by our laboratory to differentiate into both epithelial and myofibroblastic cell types. Our results indicated a clear decrease in the expression of the epithelial marker SFTPC, but our small sample size offer little evidence of increased myofibroblast activity. Taken together, there is still much to elucidate on the role of cigarette smoke and the conditions that trigger a variety of pulmonary diseases. An increase in the sample size might provide more evidence for a role of cigarette smoke and redirected stem cell differentiation in IPF.
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