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Am J Physiol Renal Physiol 282: F910-F920, 2002. First published November 20, 2001; doi:10.1152/ajprenal.00252.2001
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Vol. 282, Issue 5, F910-F920, May 2002

TGF-beta -induced Ca2+ influx involves the type III IP3 receptor and regulates actin cytoskeleton

Tracy A. McGowan1, Muniswamy Madesh2, Yanqing Zhu1, Lewei Wang1, Mark Russo1, Leo Deelman3, Rob Henning3, Suresh Joseph2, Gyorgy Hajnoczky2, and Kumar Sharma1

1 Dorrance Hamilton Laboratories, Division of Nephrology, Department of Medicine, and 2 Department of Anatomy, Pathology, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107; and 3 Department of Clinical Pharmacology, University of Groningen, 9713 AV Groningen, The Netherlands

Ca2+ influx has been postulated to modulate the signaling pathway of transforming growth factor-beta (TGF-beta ); however, the underlying mechanism and functional significance of TGF-beta -induced stimulation of Ca2+ influx are unclear. We show here that TGF-beta stimulates Ca2+ influx in mesangial cells without Ca2+ release. The influx of Ca2+ is prevented by pharmacological inhibitors of inositol 1,4,5-trisphosphate receptors (IP3R) as well as specific antibodies to type III IP3R (IP3RIII) but not to type I IP3R (IP3RI). TGF-beta enhances plasma membrane localization of IP3RIII, whereas the sarcoplasmic-endoplasmic reticulum Ca2+-ATPase (SERCA) preferentially translocates to the nucleus. Untreated mesangial cells exhibit actin filamentous protrusions on the cell surface, and treatment with TGF-beta dramatically reduces this pattern. The alterations in the actin cytoskeleton by TGF-beta are dependent on TGF-beta -induced Ca2+ influx. These studies identify a novel pathway by which TGF-beta regulates Ca2+ influx and induces cytoskeletal alterations.

mesangial cells; signaling; filipodia; inositol 1,4,5-trisphosphate; transforming growth factor-beta


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