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This Article Full Text Full Text (PDF) All Versions of this Article: 286/2/F356    most recent 00138.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Kanellis, J. Articles by Sheikh-Hamad, D. Search for Related Content PubMed PubMed Citation Articles by Kanellis, J. Articles by Sheikh-Hamad, D.

Stanniocalcin-1, an inhibitor of macrophage chemotaxis and chemokinesis

¹The Renal Section, ⁴Renal Pathology Laboratory, Department of Pathology, Baylor College of Medicine, ³Department of Pathology, University of Texas Health Sciences Center, Houston, Texas 77030; and ²Kidney Laboratory, Austin Research Institute and Department of Nephrology, Austin Hospital, University of Melbourne, Australia 3084

Submitted 4 April 2003 ; accepted in final form 7 October 2003

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) 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. Consistent with these findings, STC1 blunted the rise in intracellular calcium following MCP-1 stimulation in RAW264.7 cells. In vivo studies suggested differential expression of STC1 in obstructed kidney and localization to macrophages. MCP-1 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.

monocyte chemotactic protein-1; stromal cell-derived factor-1; ureteric obstruction; calcium homeostasis; kidney injury

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