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3Renal Section, Department of Medicine, and 1Leukocyte Biology, Children's Nutritional Research Center, Baylor College of Medicine, 4Department of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, and 5Department of Renal Pathology, Methodist Hospital, Houston, Texas; and 2Department of Physiology, University of Arizona, Tucson, Arizona
Submitted 14 June 2006 ; accepted in final form 3 October 2006
The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) inhibits monocyte chemotactic protein-1- and stromal-derived factor-1
(SDF-1
)-mediated chemotaxis and diminishes chemokinesis in macrophage-like RAW264.7 and U937 cells in a manner that may involve attenuation of the intracellular calcium signal. STC1 is strongly induced in the kidney following obstructive injury. We hypothesized that STC1 may serve to attenuate the influx of inflammatory cells to the site of tissue injury. In this study, we examined the effect of STC1 on the migration of freshly isolated human macrophages, neutrophils, and T and B lymphocytes through quiescent or IL-1
-treated human umbilical vein endothelial cell (HUVEC) monolayers. STC1 inhibited transmigration of macrophages and T lymphocytes through quiescent or IL-1
-activated HUVECs but did not attenuate the transmigration of neutrophils and B lymphocytes. STC1 regulates gene expression in cultured endothelial cells and is detected on the apical surface of endothelial cells in vivo. The data suggest that STC1 plays a critical role in transendothelial migration of inflammatory cells and is involved in the regulation of numerous aspects of endothelial function.
array; inflammation; vascular biology; calcium regulation
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