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Fluid shear stress was found to drive gene expression in endothelial and endocardial cells and is consequently believed to play a role in cardiovascular development Extensive remodeling during cardiovascular development alters patterns of this hemodynamic force considerably. The mechanism by which endothelial cells sense these alterations in fluid shear stress remains to be revealed. In this study we postulate a role for primary cilia as fluid shear stress sensors of endothelial cells. Such a function has already been attributed to primary cilia on epithelial cells of the adult kidney and Hensen's node in the embryo, where the mechanical signal is transduced into an intracellular Ca2+ signaling response. A comparable mechanism of shear stress sensing by endothelial cells is conceivable. Recently, primary cilia were observed on cultured human umbilical vein endothelial cells. These primary cilia disassembled when exposed to high levels of shear stress. Endocardial cells were found to be more shear responsive than endothelial cells. Nevertheless, primary cilia have, thus far, not been detected on endocardial cells. In the present study, we show a shear stress related distribution of cellular protrusions within the cardiovasculature of the chicken embryo with field emission scanning electron microscopy. We identify one of these cellular protrusions as a monocilium by fluorescent staining with monoclonal antibodies directed against acetylated or detyrosinated isoforms of alpha tubulin. The distribution pattern of these monocilia is compared to the expression pattern of Krüppel-like factor-2; a high shear stress marker. We demonstrate the presence of monocilia on endocardial cells in low shear stress regions and postulate that they are primary cilia, which function as fluid shear stress sensors.
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J. Vasc. Biol. 42, Sup:2 (2005) p59