Synthesis of prostaglandins in cholera toxin-treated Chinese hamster ovary cells

Johnny Peterson, Christopher A. Jackson, James C. Reitmeyer

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The prostaglandin (PG) and adenosine 3′,5′-cyclic monophosphate (cAMP) responses of Chinese hamster ovary (CHO) cells were measured after cholera toxin (CT) exposure to evaluate dose and kinetic relationships. Release of prostaglandin E2 (PGE2) and the accumulation of cAMP were dependent on the dose of CT, with an effective dose of approximately 10-100 ng/ml within 4 h; the PGE2 response was about four- to six-fold more than that of PGE1. CHO cells exposed to CT also released increased amounts of thromboxane B2 (TxB2), PGF, and 6-keto PGF (a non-enzymatic degradation product of prostacyclin). Kinetic analysis of CT-treated cells revealed that small peaks of cAMP accumulation and of PGE1 and PGE2 release were detected at approximately 30 min, but larger, progressive PG and cAMP responses were measured 2-4 h later. Exposure of the cells to relatively high doses of membrane-permeable derivatives of cAMP (1 mm) and forskolin (10 μm) caused PGE2 release. Concomitantly, exogenous PGE2 (100 μm) increased intraceliular levels of cAMP. We have considered the interrelationship of the cyclo-oxygenase and the cyclic nucleotide pathways relative to the molecular mechanism of CT.

Original languageEnglish (US)
Pages (from-to)345-353
Number of pages9
JournalMicrobial Pathogenesis
Volume9
Issue number5
DOIs
StatePublished - 1990

Fingerprint

Cholera Toxin
Cricetulus
Dinoprostone
Prostaglandins
Ovary
Alprostadil
Thromboxane B2
Dinoprost
Cyclic Nucleotides
Colforsin
Epoprostenol
Prostaglandin-Endoperoxide Synthases
Adenosine
Membranes

Keywords

  • cAMP
  • CHO cells
  • cholera toxin
  • prostaglandins

ASJC Scopus subject areas

  • Microbiology
  • Infectious Diseases

Cite this

Synthesis of prostaglandins in cholera toxin-treated Chinese hamster ovary cells. / Peterson, Johnny; Jackson, Christopher A.; Reitmeyer, James C.

In: Microbial Pathogenesis, Vol. 9, No. 5, 1990, p. 345-353.

Research output: Contribution to journalArticle

Peterson, Johnny ; Jackson, Christopher A. ; Reitmeyer, James C. / Synthesis of prostaglandins in cholera toxin-treated Chinese hamster ovary cells. In: Microbial Pathogenesis. 1990 ; Vol. 9, No. 5. pp. 345-353.
@article{2fe91ef71efd4a3ab8b5a94a25c0ee28,
title = "Synthesis of prostaglandins in cholera toxin-treated Chinese hamster ovary cells",
abstract = "The prostaglandin (PG) and adenosine 3′,5′-cyclic monophosphate (cAMP) responses of Chinese hamster ovary (CHO) cells were measured after cholera toxin (CT) exposure to evaluate dose and kinetic relationships. Release of prostaglandin E2 (PGE2) and the accumulation of cAMP were dependent on the dose of CT, with an effective dose of approximately 10-100 ng/ml within 4 h; the PGE2 response was about four- to six-fold more than that of PGE1. CHO cells exposed to CT also released increased amounts of thromboxane B2 (TxB2), PGF2α, and 6-keto PGF1α (a non-enzymatic degradation product of prostacyclin). Kinetic analysis of CT-treated cells revealed that small peaks of cAMP accumulation and of PGE1 and PGE2 release were detected at approximately 30 min, but larger, progressive PG and cAMP responses were measured 2-4 h later. Exposure of the cells to relatively high doses of membrane-permeable derivatives of cAMP (1 mm) and forskolin (10 μm) caused PGE2 release. Concomitantly, exogenous PGE2 (100 μm) increased intraceliular levels of cAMP. We have considered the interrelationship of the cyclo-oxygenase and the cyclic nucleotide pathways relative to the molecular mechanism of CT.",
keywords = "cAMP, CHO cells, cholera toxin, prostaglandins",
author = "Johnny Peterson and Jackson, {Christopher A.} and Reitmeyer, {James C.}",
year = "1990",
doi = "10.1016/0882-4010(90)90068-2",
language = "English (US)",
volume = "9",
pages = "345--353",
journal = "Microbial Pathogenesis",
issn = "0882-4010",
publisher = "Academic Press Inc.",
number = "5",

}

TY - JOUR

T1 - Synthesis of prostaglandins in cholera toxin-treated Chinese hamster ovary cells

AU - Peterson, Johnny

AU - Jackson, Christopher A.

AU - Reitmeyer, James C.

PY - 1990

Y1 - 1990

N2 - The prostaglandin (PG) and adenosine 3′,5′-cyclic monophosphate (cAMP) responses of Chinese hamster ovary (CHO) cells were measured after cholera toxin (CT) exposure to evaluate dose and kinetic relationships. Release of prostaglandin E2 (PGE2) and the accumulation of cAMP were dependent on the dose of CT, with an effective dose of approximately 10-100 ng/ml within 4 h; the PGE2 response was about four- to six-fold more than that of PGE1. CHO cells exposed to CT also released increased amounts of thromboxane B2 (TxB2), PGF2α, and 6-keto PGF1α (a non-enzymatic degradation product of prostacyclin). Kinetic analysis of CT-treated cells revealed that small peaks of cAMP accumulation and of PGE1 and PGE2 release were detected at approximately 30 min, but larger, progressive PG and cAMP responses were measured 2-4 h later. Exposure of the cells to relatively high doses of membrane-permeable derivatives of cAMP (1 mm) and forskolin (10 μm) caused PGE2 release. Concomitantly, exogenous PGE2 (100 μm) increased intraceliular levels of cAMP. We have considered the interrelationship of the cyclo-oxygenase and the cyclic nucleotide pathways relative to the molecular mechanism of CT.

AB - The prostaglandin (PG) and adenosine 3′,5′-cyclic monophosphate (cAMP) responses of Chinese hamster ovary (CHO) cells were measured after cholera toxin (CT) exposure to evaluate dose and kinetic relationships. Release of prostaglandin E2 (PGE2) and the accumulation of cAMP were dependent on the dose of CT, with an effective dose of approximately 10-100 ng/ml within 4 h; the PGE2 response was about four- to six-fold more than that of PGE1. CHO cells exposed to CT also released increased amounts of thromboxane B2 (TxB2), PGF2α, and 6-keto PGF1α (a non-enzymatic degradation product of prostacyclin). Kinetic analysis of CT-treated cells revealed that small peaks of cAMP accumulation and of PGE1 and PGE2 release were detected at approximately 30 min, but larger, progressive PG and cAMP responses were measured 2-4 h later. Exposure of the cells to relatively high doses of membrane-permeable derivatives of cAMP (1 mm) and forskolin (10 μm) caused PGE2 release. Concomitantly, exogenous PGE2 (100 μm) increased intraceliular levels of cAMP. We have considered the interrelationship of the cyclo-oxygenase and the cyclic nucleotide pathways relative to the molecular mechanism of CT.

KW - cAMP

KW - CHO cells

KW - cholera toxin

KW - prostaglandins

UR - http://www.scopus.com/inward/record.url?scp=0025615481&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025615481&partnerID=8YFLogxK

U2 - 10.1016/0882-4010(90)90068-2

DO - 10.1016/0882-4010(90)90068-2

M3 - Article

VL - 9

SP - 345

EP - 353

JO - Microbial Pathogenesis

JF - Microbial Pathogenesis

SN - 0882-4010

IS - 5

ER -