Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 477, Issue 2, Pages 244-252Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2008.06.019
Keywords
ATP; JNK; osteoblasts; P2Y(2) receptors; Ca2+; PKC; Src
Categories
Funding
- Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET)
- Agencia Nacional de Promocion Cientifica y Tecnologica
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This work shows that ATP activates JNK1, but not JNK2, in rat osteoblasts and RCS-A 17/2.8 osteoblast-like cells. In RCS-A 17/2.8 cells ATP induced JNK1 phosphorylation in a close- and time-dependent manner. JNK1 phosphorylation also increased after osteoblast stimulation with ATP gamma S and UTP, but not with ADP beta S. RT-PCR studies supported the expression of P2Y(2) receptor Subtype. ATP-induced JNK1 activation Was reduced by PI-PLC, IP3 receptor, PKC and Src inhibitors and by gadolinium, nifedipine and verapamil or a Ca2+-free medium. ERK 1/2 or p38 MAPK inhibitors diminished JNK1 activation by ATP, suggesting a cross-talk between these pathways. ATP stimulated osteoblast-like cell proliferation consistent with the participation of P2Y(2) receptors. These results show that P2Y(2) receptor Stimulation by ATP induces JNK1 phosphorylation in RCS-A 17/2.8 cells in a way dependent on PI-PLC/IP3/intracellular Ca2+ release and Ca2+ influx through stress activated and L-type voltage-dependent calcium channels and involves PKC and Src kinases. (C) 2008 Elsevier Inc. All rights reserved.
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