Ca2+/cam-dependent protein kinase ii (camk ii) mediates activation of map kinase (mapk) and cytosolic phospholipase a2(cpla2) in norepinephrine (ne) induced arachidonic acid (aa) release in rabbit vascular smooth muscle cells (VSMC)

Kafait Malik, M. M. Mutbalif, I. F. Benter, W. Al-Sibai

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Abstract

NE stimulates AA release for prostacyclin synthesis in rabbit VSMC via activation of cPLA2 bill not sPLA2 by a mechanism dependent on Ca2+ influx. The purpose of this sludy was to investigate the contribution ana relationship of CaMK II and MAPK in NE induced AA release. In VSMC pivlaheled with [3H]AA, NE (10 μM) enhanced MAPK and CaMK II activity. In cells, transiently Iransfected using lipol'ectamine with antisense, hul not sense, oligonucleotidcs (1-5 μM) complementary to the translation initiation siles of MAPK anil CaMK II, NE induced [3H]AA release was inhibited by 35% and 100% respectively. Treatment of cells with MAPK antisensc, hul not sense, oligonucleoticles abolished the NE induced MAPK activation. In cells transfecled with CaMK II antisense oligonucleotides NE induced MAPK aclivaiion was inhibited. These data suggest CaMK II is involved in the NE induced signal transduetion pathway in the release of AA in VSMC. Moreover CaMK II appears to activate MAPK which in turn stimulates cPLA2 lo release AA lor proslacyclin synthesis in the rabbit VSMC.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996

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Cytosolic Phospholipases A2
phospholipase A2
Cams
norepinephrine
arachidonic acid
Vascular Smooth Muscle
blood vessels
Arachidonic Acid
protein kinases
smooth muscle
myocytes
Protein Kinases
Smooth Muscle Myocytes
Muscle
Norepinephrine
phosphotransferases (kinases)
Phosphotransferases
Chemical activation
rabbits
Cells

All Science Journal Classification (ASJC) codes

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

@article{8a11f9ec39504811b28a35b9e6fd1870,
title = "Ca2+/cam-dependent protein kinase ii (camk ii) mediates activation of map kinase (mapk) and cytosolic phospholipase a2(cpla2) in norepinephrine (ne) induced arachidonic acid (aa) release in rabbit vascular smooth muscle cells (VSMC)",
abstract = "NE stimulates AA release for prostacyclin synthesis in rabbit VSMC via activation of cPLA2 bill not sPLA2 by a mechanism dependent on Ca2+ influx. The purpose of this sludy was to investigate the contribution ana relationship of CaMK II and MAPK in NE induced AA release. In VSMC pivlaheled with [3H]AA, NE (10 μM) enhanced MAPK and CaMK II activity. In cells, transiently Iransfected using lipol'ectamine with antisense, hul not sense, oligonucleotidcs (1-5 μM) complementary to the translation initiation siles of MAPK anil CaMK II, NE induced [3H]AA release was inhibited by 35{\%} and 100{\%} respectively. Treatment of cells with MAPK antisensc, hul not sense, oligonucleoticles abolished the NE induced MAPK activation. In cells transfecled with CaMK II antisense oligonucleotides NE induced MAPK aclivaiion was inhibited. These data suggest CaMK II is involved in the NE induced signal transduetion pathway in the release of AA in VSMC. Moreover CaMK II appears to activate MAPK which in turn stimulates cPLA2 lo release AA lor proslacyclin synthesis in the rabbit VSMC.",
author = "Kafait Malik and Mutbalif, {M. M.} and Benter, {I. F.} and W. Al-Sibai",
year = "1996",
language = "English (US)",
volume = "10",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "3",

}

TY - JOUR

T1 - Ca2+/cam-dependent protein kinase ii (camk ii) mediates activation of map kinase (mapk) and cytosolic phospholipase a2(cpla2) in norepinephrine (ne) induced arachidonic acid (aa) release in rabbit vascular smooth muscle cells (VSMC)

AU - Malik, Kafait

AU - Mutbalif, M. M.

AU - Benter, I. F.

AU - Al-Sibai, W.

PY - 1996

Y1 - 1996

N2 - NE stimulates AA release for prostacyclin synthesis in rabbit VSMC via activation of cPLA2 bill not sPLA2 by a mechanism dependent on Ca2+ influx. The purpose of this sludy was to investigate the contribution ana relationship of CaMK II and MAPK in NE induced AA release. In VSMC pivlaheled with [3H]AA, NE (10 μM) enhanced MAPK and CaMK II activity. In cells, transiently Iransfected using lipol'ectamine with antisense, hul not sense, oligonucleotidcs (1-5 μM) complementary to the translation initiation siles of MAPK anil CaMK II, NE induced [3H]AA release was inhibited by 35% and 100% respectively. Treatment of cells with MAPK antisensc, hul not sense, oligonucleoticles abolished the NE induced MAPK activation. In cells transfecled with CaMK II antisense oligonucleotides NE induced MAPK aclivaiion was inhibited. These data suggest CaMK II is involved in the NE induced signal transduetion pathway in the release of AA in VSMC. Moreover CaMK II appears to activate MAPK which in turn stimulates cPLA2 lo release AA lor proslacyclin synthesis in the rabbit VSMC.

AB - NE stimulates AA release for prostacyclin synthesis in rabbit VSMC via activation of cPLA2 bill not sPLA2 by a mechanism dependent on Ca2+ influx. The purpose of this sludy was to investigate the contribution ana relationship of CaMK II and MAPK in NE induced AA release. In VSMC pivlaheled with [3H]AA, NE (10 μM) enhanced MAPK and CaMK II activity. In cells, transiently Iransfected using lipol'ectamine with antisense, hul not sense, oligonucleotidcs (1-5 μM) complementary to the translation initiation siles of MAPK anil CaMK II, NE induced [3H]AA release was inhibited by 35% and 100% respectively. Treatment of cells with MAPK antisensc, hul not sense, oligonucleoticles abolished the NE induced MAPK activation. In cells transfecled with CaMK II antisense oligonucleotides NE induced MAPK aclivaiion was inhibited. These data suggest CaMK II is involved in the NE induced signal transduetion pathway in the release of AA in VSMC. Moreover CaMK II appears to activate MAPK which in turn stimulates cPLA2 lo release AA lor proslacyclin synthesis in the rabbit VSMC.

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