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

Tracy A. McGowan, Muniswamy Madesh, Yanqing Zhu, Lewei Wang, Mark Russo, Leo Deelman, Rob Henning, Suresh Joseph, Gyorgy Hajnoczky, Kumar Sharma

Producción científica: Articlerevisión exhaustiva

42 Citas (Scopus)


Ca2+ influx has been postulated to modulate the signaling pathway of transforming growth factor-β (TGF-β); however, the underlying mechanism and functional significance of TGF-β-induced stimulation of Ca2+ influx are unclear. We show here that TGF-β 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-β enhances plasma membrane localization of IP3RIII, whereas the sarcoplasmicendoplasmic reticulum Ca2+-ATPase (SERCA) preferentially translocates to the nucleus. Untreated mesangial cells exhibit actin filamentous protrusions on the cell surface, and treatment with TGF-β dramatically reduces this pattern. The alterations in the actin cytoskeleton by TGF-β are dependent on TGF-β-induced Ca2+ influx. These studies identify a novel pathway by which TGF-β regulates Ca2+ influx and induces cytoskeletal alterations.

Idioma originalEnglish (US)
Páginas (desde-hasta)F910-F920
PublicaciónAmerican Journal of Physiology - Renal Physiology
N.º5 51-5
EstadoPublished - 2002
Publicado de forma externa

ASJC Scopus subject areas

  • Physiology
  • Urology


Profundice en los temas de investigación de 'TGF-β-induced Ca2+ influx involves the type III IP3 receptor and regulates actin cytoskeleton'. En conjunto forman una huella única.

Citar esto