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Example sentences for: cell-
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Additionally, C-reactive protein reduces endothelial nitric oxide synthase, upregulates the proatherosclerotic NF-κB pathway, enhances low-density lipoprotein (LDL) uptake by macrophages, which become foam cells, and facilitates T-cell- and complement-mediated destruction and apoptosis of the endothelium [2,26,29–31].
It is generally accepted that the driving force for cell movement is provided by the dynamic reorganization of the actin cytoskeleton, directing protrusion (lamellipodia and filopodia) at the front of the cell and retraction at the rear [ 30 31 ] . Although we have not examined the ultrastructure of the dermal fibroblasts at the edge of wound sites, we showed previously by electron microscopy that in the lens of SPARC-null mice numerous cellular processes extended into the ECM of the lens capsule [ 23 ] . We further showed that, in contrast to the abnormal filopodial projections at the lens cell-ECM interface, cell-cell contacts between the neighboring lens epithelial cells and between the lens epithelial and fiber cells were normal [ 23 ] . The results indicate that disassembly of cell-cell contacts between lens cells is not taking place, despite the forward movement of the lens cells into the ECM of the capsule.
[ 3 4 ] ), and tumorigenesis [ 5 6 ] . SPARC belongs to a class of recently denoted matricellular proteins that are involved in cell-ECM interactions.
Regan, University of Arizona) was used for immunocytochemical confirmation of protein expression in isolated thin limbs of Henle as described previously [ 30 ] . Tubules were positioned onto a glass microscope slide covered with a layer of Cell-Tak ®adhesive (Becton Dickinson, Bedford, MA).
Previously, studies of phenotypes in this laboratory have shown that SPARC-null mice develop osteopenia around 2.5 months of age [ 19 ] in bones where SPARC is normally the most abundant non-collagenous glycoprotein [ 3 ] . The second phenotype thus far uncovered is in the lens where SPARC is normally produced by lens epithelial cells [ 20 21 ] and is a component of the lens capsule [ 20 22 ] . SPARC-null mice show progressive cataract formation beginning approximately 1.5 months after birth [ 14 21 ] . Electron microscopy of the SPARC-null lens revealed abnormality at the lens cell-ECM (capsule) interface with an intrusion of cellular processes into the basement membrane of the lens capsule, whereas wild-type lens exhibited a precise border at the cell-matrix interface [ 23 ] . In the present study, we show for the first time that SPARC plays a role in wound repair in vivo and in vitro.
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