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Papers In Press, published online ahead of print December 6, 2003
Bioquímica y Biología Molecular, Universidad de Chile, Facultad Ciencias Químicas y Farmacéuticas, Santiago 664 0750
Corresponding Author: slavander{at}uchile.cl
In the heart, insulin-like growth factor-1 (IGF-1) is a pro-hypertrophic and anti apoptotic peptide. In cultured rat cardiomyocytes, IGF-1 induced a fast and transient increase in Ca2+i levels apparent both in nucleus and cytosol, releasing this ion from intracellular stores through an inositol-1,4,5-trisphosphate (IP3) dependent signaling pathway. Intracellular IP3 levels increased after stimulation by IGF-1 both in presence and absence of extracellular Ca2+. A different spatial distribution of IP3 receptor isoforms in cardiomyocytes was found. Ryanodine did not prevent the IGF 1 induced increase of Ca2+i levels but inhibited the basal and spontaneous Ca2+i oscillations observed when cardiac myocytes were incubated in Ca2+-containing resting media. Spatial analysis of fluorescence images of IGF-1-stimulated cardiomyocytes incubated in Ca2+-containing resting media showed an early increase in Ca2+i, initially localized in the nucleus. Calcium imaging suggested that part of Ca2+ released by stimulation with IGF-1 was initially contained in the perinuclear region. The IGF-1-induced increase on Ca2+i levels was prevented by BAPTA-AM, thapsigargin, xestospongin C, 2-amino ethoxydiphenyl borate, U-73122, pertussis toxin and
J. Biol. Chem, 10.1074/jbc.M311604200
Submitted on October 22, 2003
Revised on December 1, 2003
Accepted on December 6, 2003
Insulin like growth factor-1 induces an inositol 1,4,5-trisphosphate-dependent increase in nuclear and cytosolic calcium in cultured rat cardiac myocytes
ARKct (a peptide inhibitor of G
signalling). Pertussis toxin also prevented the IGF-1-dependent IP3 mass increase. Genistein treatment largely decreased the IGF-1 induced changes in both Ca2+i and IP3. LY29402 (but not PD98059) also prevented the IGF-1 dependent Ca2+i increase. Both pertussis toxin and U73122 prevented the IGF-1 dependent induction of both ERKs and PKB. We conclude that IGF-1 increases Ca2+i levels in cultured cardiac myocytes through a G subunit of a pertussis toxin-sensitive G protein - PI3K - phospholipase C signaling pathway that involves participation of IP3.
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