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1 The Renal Section, Baylor College of Medicine, Houston, Texas, USA; Austin Research Institute and Department of Nephrology, University of Melbourne, Austin Hosptal, Melbourne, Australia
2 Department of Pathology, University of Texas Health Sciences Center, Houston, Texas, USA
3 The Renal Section, Baylor College of Medicine, Houston, Texas, USA
4 Renal Pathology Laboratory, Department of Pathology, Baylor College of Medicine, Houston, Texas, USA
5 Austin Research Institute and Department of Nephrology, University of Melbourne, Austin Hosptal, Melbourne, Australia
* To whom correspondence should be addressed. E-mail: sheikh{at}bcm.tmc.edu.
In macrophages, changes in intracellular calcium have been associated with activation of cellular processes that regulate cell adhesion and motility, and are important for the response of macrophages to antigenic stimuli. The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1)1 is expressed in multiple organs including the thymus and spleen, and hence, we hypothesized that it may have a role in modulating the immune/inflammatory response. Using murine macrophage-like (RAW264.7) and human monoblast-like (U937) cells to study chemotaxis in vitro, we found that STC1 attenuated chemokinesis and diminished the chemotactic response to monocyte chemotactic protein-1 (MCP-1) and stromal cell-derived factor - 1 alpha (SDF-1
). Consistent with these findings, STC1 blunted the rise in intracellular calcium following MCP1 stimulation in RAW264.7 cells. In vivo studies suggested differential expression of STC1 in obstructed kidney and localization to macrophages. MCP1 and STC1 transcripts were both upregulated following ureteric obstruction, suggesting a functional association between the two genes. Our data suggest a role for mammalian STC1 in modulating the immune/inflammatory response.
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