Dr. Craig Henke and colleagues at the University of Minnesota, Minneapolis, MN propose that low levels of caveolin-1 contribute to the over-proliferation of fibroblasts in lung disease.
These results are presented in the June 2010 issue of The American Journal of Pathology.
Idiopathic pulmonary fibrosis (IPF) is a form of lung disease characterized by lung fibrosis, or development of excessive connective tissue resulting in lung damage, of unknown origin. Low levels of PTEN (phosphatase and tensin homolog), a molecule that prevents cells from growing and dividing too rapidly, have been implicated in the over-proliferation of fibroblasts following tissue injury. However, the molecular mechanisms underlying the low expression of PTEN in lung fibroblasts in IPF remain to be determined.
Xia et al hypothesized that caveolin-1, a molecule involved in cell signaling and intake of external molecules that is decreased in fibroblasts in IPF patients, may be responsible for the levels of PTEN expression in these cells. They correlated low levels of caveolin-1 and PTEN expression and demonstrated that overexpression of caveolin-1 restored PTEN expression in IPF fibroblasts. Indeed, PTEN interacted with caveolin-1 through its caveolin-1 binding sequence. Decreased caveolin-1 expression therefore facilitates the over-proliferation of fibroblasts in IPF.
Dr. Henke's group "demonstrate[s] that in IPF fibroblasts, a lack of caveolin-1 expression in the plasma membrane reduces membrane-associated PTEN levels and activity. … This confers IPF fibroblasts with a phenotype characterized by the ability to circumvent the proliferation-suppressive properties of polymerized type I collagen."
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