Title : P2Y receptors activate MAPK/ERK through a pathway involving PI3K/PDK1/PKC-zeta in human vein endothelial cells.

Pub. Date : 2006

PMID : 16914897






6 Functional Relationships(s)
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1 RESULTS: ATP, 2-meSATP, UTP and UDP cause a rapid and transitory increase in the phosphorylation of MAPK/ERK. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens
2 ATP-dependent activation of MAPK/ERK was prevented by pretreatment of HUVEC with pertussis toxin or MEK inhibitor PD98059. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens
3 In addition, activation of the MAPK/ ERK cascade by ATP was blocked in cells pretreated with wortmannin and LY294002, but not by U73122, BAPTA or a Ca(2+)-free medium. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens
4 Furthermore, an inhibition of ATP-dependent MAPK/ERK phosphorylation was observed in HUVEC pretreated with high doses of GF109203X or myristoylated PKC- zeta pseudosubstrate. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens
5 However, ATP-stimulated MAPK/ERK activation was unaffected in cells pretreated with AG1478 or perillic acid. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens
6 CONCLUSION: These observations suggest that the effects mediated by ATP in HUVEC occur via PTX-sensitive G-protein-coupled P2Y receptors through PI3K-dependent mechanisms, in which PDK1 and PKC-zeta are two key molecules within signal cascade leading to MAPK/ERK activation. Adenosine Triphosphate mitogen-activated protein kinase 1 Homo sapiens