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Articles in PresS, published online ahead of print November 20, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00252.2001
Submitted on August 15, 2001
Accepted on November 14, 2001
1 Medicine, Thomas Jefferson University, Philadelphia, PA, USA
2 Anatomy, Cell Biology and Pathology, Thomas Jefferson University, Philadelphia, PA, USA
3 Clinical Pharmacology, University of Groningen, Groningen, Groningen, Netherlands
* To whom correspondence should be addressed. E-mail: kumar.sharma{at}mail.tju.edu.
Calcium influx has been postulated to modulate the signaling pathway of Transforming Growth Factor-beta (TGF-ß), however the underlying mechanism and functional significance of TGF-ß-induced stimulation of Ca2+ influx is unclear. We show here that TGF-ß stimulates Ca2+ influx in mesangial cells without Ca2+ release. The influx of Ca2+ is prevented by pharmacologic inhibitors of inositol 1,4,5-trisphosphate receptors (IP3R) as well as specific antibodies to the type III IP3R (IP3RIII) but not to type I IP3R (IP3RI). TGF-ß enhances plasma membrane localization of IP3RIII whereas the sarcoplasmic-endoplasmic reticulum Ca-ATPase (SERCA) preferentially translocates to the nucleus. Untreated mesangial cells exhibit actin filamentous protrusions on the cell surface and treatment with TGF-ß dramatically reduces this pattern. The alterations in the actin cytoskeleton by TGF-ß are dependent on TGF-ß-induced Ca2+ influx. These studies identify a novel pathway by which TGF-ß regulates calcium influx and induces cytoskeletal alterations.
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