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Biochem Pharmacol 2006, PMID: 16643859

Cross-talk between angiotensin II and glucagon receptor signaling mediates phosphorylation of mitogen-activated protein kinases ERK 1/2 in rat glomerular mesangial cells.

Li, Xiao C; Carretero, Oscar A; Zhuo, Jia L

We have recently shown that the pancreatic hormone glucagon-induced phosphorylation of mitogen-activated protein (MAP) kinase ERK 1/2 as well as growth and proliferation of rat glomerular mesangial cells (MCs) via activation of cAMP-dependent protein kinase A (PKA)- and phospholipase C (PLC)/Ca2+-mediated signaling pathways. Since circulating glucagon and tissue angiotensin II (Ang II) levels are inappropriately elevated in type 2 diabetes, we tested the hypothesis that glucagon induces phosphorylation of ERK 1/2 in MCs by interacting with Ang II receptor signaling. Stimulation of MCs by glucagon (10 nM) induced a marked increase in intracellular [Ca2+]i that was abolished by [Des-His1, Glu9]-glucagon (1 microM), a selective glucagon receptor antagonist. Both glucagon and Ang II-induced ERK 1/2 phosphorylation (glucagon: 214+/-14%; Ang II: 174+/-16%; p<0.001 versus control), and these responses were inhibited by the AT1 receptor blocker losartan (glucagon + losartan: 77+/-14%; Ang II + losartan: 84+/-18%; p<0.01 versus glucagon or Ang II) and the AT2 receptor blocker PD 123319 (glucagon + PD: 78+/-7%; Ang II + PD: 87+/-7%; p<0.01 versus glucagon or Ang II). Inhibition of cAMP-dependent PKA with H89 (1 microM) or PLC with U73122 (1 microM) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon (glucagon + U73122: 109+/-15%; glucagon + H89: 113+/-16%; p<0.01 versus glucagon) or Ang II (Ang II + U73122: 111+/-13%; Ang II + H89: 86+/-10%; p<0.01 versus Ang II). Wortmannin (1 microM), a selective PI 3-kinase inhibitor, also blocked glucagon- or Ang II-induced ERK 1/2 phosphorylation. These results suggest that AT1 receptor-activated cAMP-dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon-induced MAP kinase ERK 1/2 phosphorylation in MCs. The inhibitory effect of PD 123319 on glucagon-induced ERK 1/2 phosphorylation further suggests that AT2 receptors also play a similar role in this response.

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Text Mining Data

ERK 1/2 → glucagon: " We have recently shown that the pancreatic hormone glucagon induced phosphorylation of mitogen activated protein ( MAP ) kinase ERK 1/2 as well as growth and proliferation of rat glomerular mesangial cells (MCs) via activation of cAMP dependent protein kinase A (PKA)- and phospholipase C (PLC)/Ca2+ mediated signaling pathways "

ERK 1/2 → glucagon: " We have recently shown that the pancreatic hormone glucagon induced phosphorylation of mitogen activated protein ( MAP ) kinase ERK 1/2 as well as growth and proliferation of rat glomerular mesangial cells (MCs) via activation of cAMP dependent protein kinase A (PKA)- and phospholipase C (PLC)/Ca2+ mediated signaling pathways "

MCs → glucagon: " Since circulating glucagon and tissue angiotensin II (Ang II) levels are inappropriately elevated in type 2 diabetes, we tested the hypothesis that glucagon induces phosphorylation of ERK 1/2 in MCs by interacting with Ang II receptor signaling "

ERK 1/2 → glucagon: " Since circulating glucagon and tissue angiotensin II (Ang II) levels are inappropriately elevated in type 2 diabetes, we tested the hypothesis that glucagon induces phosphorylation of ERK 1/2 in MCs by interacting with Ang II receptor signaling "

ERK 1/2 → glucagon: " Since circulating glucagon and tissue angiotensin II (Ang II) levels are inappropriately elevated in type 2 diabetes, we tested the hypothesis that glucagon induces phosphorylation of ERK 1/2 in MCs by interacting with Ang II receptor signaling "

Ca2+ → MCs: " Stimulation of MCs by glucagon ( 10 nM ) induced a marked increase in intracellular [ Ca2+ ] i that was abolished by [ Des-His1, Glu9 ] -glucagon ( 1 microM ), a selective glucagon receptor antagonist "

Ca2+ → glucagon: " Stimulation of MCs by glucagon ( 10 nM ) induced a marked increase in intracellular [ Ca2+ ] i that was abolished by [ Des-His1, Glu9 ] -glucagon ( 1 microM ), a selective glucagon receptor antagonist "

MCs → glucagon: " Stimulation of MCs by glucagon ( 10 nM ) induced a marked increase in intracellular [ Ca2+ ] i that was abolished by [ Des-His1, Glu9 ] -glucagon ( 1 microM ), a selective glucagon receptor antagonist "

ERK 1/2 → glucagon: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

ERK 1/2 → Ang II: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

ERK 1/2 → PKA: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

ERK 1/2 → glucagon: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

ERK 1/2 → Ang II: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

ERK 1/2 → PKA: " Inhibition of cAMP dependent PKA with H89 ( 1 microM ) or PLC with U73122 ( 1 microM ) also markedly attenuated the phosphorylation of ERK 1/2 induced by glucagon ( glucagon + U73122 : 109+/-15 % ; glucagon + H89 : 113+/-16 % ; p < 0.01 versus glucagon ) or Ang II ( Ang II + U73122 : 111+/-13 % ; Ang II + H89 : 86+/-10 % ; p < 0.01 versus Ang II ) "

MCs → AT1: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

MCs → glucagon: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

ERK 1/2 → AT1: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

ERK 1/2 → glucagon: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

ERK 1/2 → AT1: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

ERK 1/2 → glucagon: " These results suggest that AT1 receptor activated cAMP dependent PKA, PLC and PI 3-kinase signaling is involved in glucagon induced MAP kinase ERK 1/2 phosphorylation in MCs "

ERK 1/2 → glucagon: " The inhibitory effect of PD 123319 on glucagon induced ERK 1/2 phosphorylation further suggests that AT2 receptors also play a similar role in this response "

ERK 1/2 → glucagon: " The inhibitory effect of PD 123319 on glucagon induced ERK 1/2 phosphorylation further suggests that AT2 receptors also play a similar role in this response "

Manually curated Databases

No curated data.