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1 Pediatrics-Leukocyte Biology, Baylor College of Medicine, Houston, Texas, United States
2 Physiology, University of Arizona, Tucson, Arizona, United States
3 Renal Division/Medicine, Baylor College of Medicine, Houston, Texas, United States
4 Departments of Pediatrics, Immunology, and Medicine, Baylor College of Medicine, Houston, Texas, United States
5 Houston, Texas, United States; Pathology, University of Texas Health Science Center, Houston, Texas, United States
6 Pathology, Methodist Hospital, Houston, Texas, United States
7 Pathology, University of Texas Health Science Center, Houston, Texas, United States
* To whom correspondence should be addressed. E-mail: sheikh{at}bcm.tmc.edu.
The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) inhibits monocyte chemotactic protein-1 (MCP-1) and stromal-derived factor-1
(SDF-1)-mediated chemotaxis and diminishes chemokinesis in the macrophage-like, RAW264.7 and U937 cells, in a manner that may involve attenuation of 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, 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 trans-endothelial migration of inflammatory cells and is involved in the regulation of numerous aspects of endothelial function.
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