Abstract
Epithelial mesenchymal interactions, cell proliferation, polarity, migration and differentiation are essential for proper lung branching morphogenesis. Rac1, a small Rho GTPases, plays a key role in cell polarity and cell migration. Therefore, we hypothesize that Rac1 controls branching morphogenesis during embryonic lung development. We used an in vitro lung culture model to assess the effect of NSC23766, a Rac1 inhibitor, on lung branching. Using 50μM (IC50) of Rac1 inhibitor, we observed a decrease in branching and necrosis of the tissue at 48 hrs. At 25 μM, Rac1 inhibitor decreased branching without necrosis. This decrease was accompanied with a reduction in cell proliferation. Furthermore, using Wnt reporter, TOPGAL, Rac1 inhibition reduced the expression of LacZ. In addition, using Flk1‐LacZ reporter, we observed a decrease in LacZ expression in presence of Rac1 inhibitor. Our data suggests that Rac1 controls epithelial and vascular morphogenesis through inhibition of Wnt signaling. Hence, dissecting the molecular pathways underlying Rac1 activity could lead to the discoveries of new therapeutic targets for arrested lung development.
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