Role of protein kinase C in NADPH oxidase derived O2*(-)-mediated regulation of KV-LVOCC axis under U46619 induced increase in [Ca2+]i in pulmonary smooth muscle cells.
Arch Biochem Biophys
; 487(2): 123-30, 2009 Jul 15.
Article
em En
| MEDLINE
| ID: mdl-19497296
ABSTRACT
Treatment of bovine pulmonary smooth muscle cells with the TxA(2) mimetic, U46619 stimulated [Ca(2+)](i), which was inhibited upon pretreatment with apocynin (NADPH oxidase inhibitor). Pretreatment with cromakalim (K(V) channel opener) or nifedepine (L-VOCC inhibitor) inhibited U46619 induced increase in [Ca(2+)](i), indicating a role of K(V)-LVOCC axis in this scenario. Neither cromakalim nor nifedepine inhibited U46619 induced increase in NADPH oxidase activity, suggesting that the NADPH oxidase activation is proximal to the K(V)-LVOCC axis in the cells. Pretreatment with calphostin C (PKC inhibitor) markedly reduced U46619 induced increase in NADPH oxidase activity and [Ca(2+)](i) in the cells. Calphostin C pretreatment also markedly reduced p(47phox) phosphorylation and translocation to the membrane and association with p(22phox), a component of Cyt.b(558) of NADPH oxidase in the membrane. Overall, PKC plays an important role in NADPH oxidase derived O(2)(-)-mediated regulation of K(V)-LVOCC axis leading to an increase in [Ca(2+)](i) by U46619 in the cells.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
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Cálcio
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Superóxidos
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NADPH Oxidases
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Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico
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Miócitos de Músculo Liso
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Canais Iônicos
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Pulmão
Limite:
Animals
Idioma:
En
Ano de publicação:
2009
Tipo de documento:
Article