Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells

Bong Hyun Ahn, Mi Hee Park, Young Han Lee, Taeg Kyu Kwon, Do Sik Min

Research output: Contribution to journalArticle

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Abstract

Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers. In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl2)-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells. CoCl2 stimulated PLD activity and synthesis of COX-2 protein in a dose and time-dependent manner. Moreover, elevated expression of PLD1 and PLD2 increased hypoxia-induced COX-2 expression and prostaglandin E2 (PGE2) production. Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed CoCl2-induced COX-2 expression and PGE2 formation. In addition, evidence that PLD activity was involved in the stimulation of COX-2 expression was provided by the observations that overexpression of wild type PLD isozymes, but not catalytically inactive PLD isozymes, stimulated CoCl2-induced COX-2 expression and PGE2 production. PLD1 enhanced COX-2 expression by CoCl2 via reactive oxygen species (ROS), p38 MAPK kinase, PKC-δ, and PKA, but not ERK, whereas PLD2 enhanced CoCl2-induced COX-2 expression via ROS and p38 MAPK, but not ERK, PKC-δ, and PKA. Differential regulation of COX-2 expression mediated through PLD isozymes was comparable with that of CoCl2-induced PLD activity in these two PLD isozymes. Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl2-induced COX-2 expression through differential signaling pathways in astroglioma cells.

Original languageEnglish
Pages (from-to)1721-1731
Number of pages11
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Volume1773
Issue number12
DOIs
Publication statusPublished - 2007 Dec 1

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Phospholipase D
Astrocytoma
Cyclooxygenase 2
Isoenzymes
Up-Regulation
Dinoprostone
p38 Mitogen-Activated Protein Kinases
Reactive Oxygen Species
cobaltous chloride
Hypoxia
Butanols
1-Butanol
Mitogen-Activated Protein Kinase Kinases
Prostaglandin-Endoperoxide Synthases
Protein Isoforms

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

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title = "Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells",
abstract = "Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers. In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl2)-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells. CoCl2 stimulated PLD activity and synthesis of COX-2 protein in a dose and time-dependent manner. Moreover, elevated expression of PLD1 and PLD2 increased hypoxia-induced COX-2 expression and prostaglandin E2 (PGE2) production. Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed CoCl2-induced COX-2 expression and PGE2 formation. In addition, evidence that PLD activity was involved in the stimulation of COX-2 expression was provided by the observations that overexpression of wild type PLD isozymes, but not catalytically inactive PLD isozymes, stimulated CoCl2-induced COX-2 expression and PGE2 production. PLD1 enhanced COX-2 expression by CoCl2 via reactive oxygen species (ROS), p38 MAPK kinase, PKC-δ, and PKA, but not ERK, whereas PLD2 enhanced CoCl2-induced COX-2 expression via ROS and p38 MAPK, but not ERK, PKC-δ, and PKA. Differential regulation of COX-2 expression mediated through PLD isozymes was comparable with that of CoCl2-induced PLD activity in these two PLD isozymes. Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl2-induced COX-2 expression through differential signaling pathways in astroglioma cells.",
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Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells. / Ahn, Bong Hyun; Park, Mi Hee; Lee, Young Han; Kwon, Taeg Kyu; Min, Do Sik.

In: Biochimica et Biophysica Acta - Molecular Cell Research, Vol. 1773, No. 12, 01.12.2007, p. 1721-1731.

Research output: Contribution to journalArticle

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T1 - Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells

AU - Ahn, Bong Hyun

AU - Park, Mi Hee

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AU - Kwon, Taeg Kyu

AU - Min, Do Sik

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N2 - Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers. In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl2)-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells. CoCl2 stimulated PLD activity and synthesis of COX-2 protein in a dose and time-dependent manner. Moreover, elevated expression of PLD1 and PLD2 increased hypoxia-induced COX-2 expression and prostaglandin E2 (PGE2) production. Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed CoCl2-induced COX-2 expression and PGE2 formation. In addition, evidence that PLD activity was involved in the stimulation of COX-2 expression was provided by the observations that overexpression of wild type PLD isozymes, but not catalytically inactive PLD isozymes, stimulated CoCl2-induced COX-2 expression and PGE2 production. PLD1 enhanced COX-2 expression by CoCl2 via reactive oxygen species (ROS), p38 MAPK kinase, PKC-δ, and PKA, but not ERK, whereas PLD2 enhanced CoCl2-induced COX-2 expression via ROS and p38 MAPK, but not ERK, PKC-δ, and PKA. Differential regulation of COX-2 expression mediated through PLD isozymes was comparable with that of CoCl2-induced PLD activity in these two PLD isozymes. Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl2-induced COX-2 expression through differential signaling pathways in astroglioma cells.

AB - Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers. In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl2)-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells. CoCl2 stimulated PLD activity and synthesis of COX-2 protein in a dose and time-dependent manner. Moreover, elevated expression of PLD1 and PLD2 increased hypoxia-induced COX-2 expression and prostaglandin E2 (PGE2) production. Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed CoCl2-induced COX-2 expression and PGE2 formation. In addition, evidence that PLD activity was involved in the stimulation of COX-2 expression was provided by the observations that overexpression of wild type PLD isozymes, but not catalytically inactive PLD isozymes, stimulated CoCl2-induced COX-2 expression and PGE2 production. PLD1 enhanced COX-2 expression by CoCl2 via reactive oxygen species (ROS), p38 MAPK kinase, PKC-δ, and PKA, but not ERK, whereas PLD2 enhanced CoCl2-induced COX-2 expression via ROS and p38 MAPK, but not ERK, PKC-δ, and PKA. Differential regulation of COX-2 expression mediated through PLD isozymes was comparable with that of CoCl2-induced PLD activity in these two PLD isozymes. Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl2-induced COX-2 expression through differential signaling pathways in astroglioma cells.

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