Prostaglandin Production by Normal and Transformed 3T3 Fibroblasts in Cell Culture

Hammarström, Sven

doi:10.1111/j.1432-1033.1977.tb11360.x

Cited by 60 publications

(19 citation statements)

References 23 publications

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“…Other primary prostaglandins represent alternative possibilities. However, E-type prostaglandins are more potent activators of adenylate cyclase in fibroblasts [27] and occur in equal or higher concentrations than other primary prostaglandins in media from cultured fibroblasts [3,7,11]. Hence, they are the most likely mediators of the rise in cyclic AMP in this system.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Claesson

Lindgren

Hammarström

1977

European Journal of Biochemistry

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High cellular adenosine 3' : 5 '-monophosphate (cyclic AMP) levels were found in a polyoma-virustransformed 3T3 fibroblast line, which produces comparatively high prostaglandin E2 concentrations. Prostaglandin E2 and cyclic AMP increased with time during 6 days of growth. Both effects were prevented by three different cyclo-oxygenase inhibitors. Addition of prostaglandin Ez, at a concentration which would have been synthesized in the absence of inhibitor, reversed the effect of indomethacin, one of the cyclo-oxygenase inhibitors, on cyclic AMP. It is concluded that endogenous prostaglandin E2 production in these transformed cells influences their cellular cyclic AMP levels.E-type prostaglandins can raise cyclic AMP levels in many tissues and cultured cells by stimulating adenylate cyclase [l]. A number of reports indicate that animal cells in culture produce prostaglandins (see e.g. [2-11 3). However, it has not been clear if this prostaglandin production has effects on cellular cyclic AMP levels since the amounts of prostaglandins produced are often orders of magnitude lower than the amounts added to raise cyclic AMP. The question if endogenous prostaglandin production can influence cyclic AMP levels in cell cultures is an important one since many reports indicate that cyclic AMP has essential roles in the regulation of cell proliferation and differentiation . The present report shows that prostaglandin E2 production by polyoma-virustransformed 3T3 cells raises their cellular cyclic AMP concentrations. MATERIALS AND METHODSDulbecco's modified Eagle's medium, calf serum, trypsin solution (2.5 %), and penicillin/streptomycin solution (10000 I.U./ml-10 mg/ml) were pur- Cell CulturesA polyoma-virus-transformed Balb/c 3T3 mouse embryo fibroblast line, originally cloned by Dr G. Todaro, was kindly given to us by Dr M. M. Burger (University of Basel, Switzerland). This cell line will be referred to as py 3T3. The cells were passaged with 0.25 % trypsin and planted at 2 x lo5 cells per 90-mm petri dish in 10 ml of Dulbecco's modified Eagle's medium containing 10% calf serum, 100 I.U./ ml of penicillin G and 0.1 mg/ml of streptomycin. Cultures were incubated at 37 "C in an atmosphere of 10% C02 in air and a relative humidity of 80%. The cells were free of mycoplasma contamination as judged by absence of cytoplasmatic incorporation of 3H-labeled thymidine [20]. All experiments were carried out in culture media containing 10% calf serum.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Claesson

Lindgren

Hammarström

1977

European Journal of Biochemistry

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“…Upon binding of hormones or other agonists to their respective cell surface receptor, AA is released from phospholipids through activation of phospholipases (1)(2)(3)(4)(5)(6)(7)(8)(9). In most if not all such instances, activation of phospholipases is associated with production of PGs and TXs (1,2,5,9,10). Therefore, it is generally believed that phospholipases control formation of PGs through release of AA.…”

Section: Introductionmentioning

confidence: 99%

“…The relation between phospholipase activation resulting in liberation of arachidonic acid (AA)' from complex glycerolipids and the cyclooxygenase pathway generating prostaglandins 1. Abbreviations used in this paper: AA, arachidonic acid; PDS, plasmaderived serum; PG, prostaglandin; PDGF, platelet-derived growth factor, TX, thromboxane.…”

Section: Introductionmentioning

confidence: 99%

Human platelet-derived growth factor stimulates prostaglandin synthesis by activation and by rapid de novo synthesis of cyclooxygenase.

Habenicht¹,

Goerig²,

Grulich³

et al. 1985

J. Clin. Invest.

212

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“…In addition, using cultured cells, it has been found that transformation by carcinogens or by viruses (Hammarstrom, 1977) is followed by increased production of PGs.…”

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confidence: 99%

Elevated levels of prostaglandin E2 in Yoshida hepatoma and the inhibition of tumour growth by non-steroidal anti-inflammatory drugs

Trevisani¹,

Ferretti²,

Capuzzo³

et al. 1980

Br J Cancer

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Summary.-Prostaglandin (PG) E2 biosynthesis in Yoshida hepatoma (AH 130) was evaluated by radioimmunoassay. When hepatoma cells were incubated in vitro, the levels of PGE2 in the medium were similar to those found in hepatocytes for the first 2 h; this was followed by a rapid increase in PGE2 formation, and the 6h incubation levels were 4-fold higher than in hepatocytes.Addition of sodium arachidonate markedly and dose-dependently stimulated PGE2 synthesis; the increase was largely prevented by the addition of indomethacin (1 um) or L 8027, a prostaglandin synthetase inhibitor.Experiments in vivo indicated that indomethacin treatment of tumour-bearing rats significantly reduced the tumour mass. When rats were injected with PGE2 after receiving the drug, the number of tumour cells was very similar to that of untreated animals. This, as well as the inhibition of tumour growth by acetylsalicylic acid, strongly suggests that the inhibition of PG biosynthesis by antiinflammatory drugs and the inhibition of tumour proliferation may be closely associated events. It was also found that injections of indomethacin very significantly prolonged survival of hepatoma-bearing rats. Since PGE2 does not appear to affect the cyclic AMP levels of hepatoma cells, it is possible that hepatoma may use PGE2 to subvert the immune system. This could help to explain the effectiveness of anti-inflammatory drugs in the control of tumour growth.

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Prostaglandin Production by Normal and Transformed 3T3 Fibroblasts in Cell Culture

Cited by 60 publications

References 23 publications

Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Human platelet-derived growth factor stimulates prostaglandin synthesis by activation and by rapid de novo synthesis of cyclooxygenase.

Elevated levels of prostaglandin E2 in Yoshida hepatoma and the inhibition of tumour growth by non-steroidal anti-inflammatory drugs

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Prostaglandin Production by Normal and Transformed 3T3 Fibroblasts in Cell Culture

Cited by 60 publications

References 23 publications

Prostaglandin E2 Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Prostaglandin E2 Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Human platelet-derived growth factor stimulates prostaglandin synthesis by activation and by rapid de novo synthesis of cyclooxygenase.

Elevated levels of prostaglandin E2 in Yoshida hepatoma and the inhibition of tumour growth by non-steroidal anti-inflammatory drugs

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Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels

Prostaglandin E₂ Production in 3T3 Cells Transformed by Polyoma Virus Raises the Intracellular Adenosine 3′: 5′‐Monophosphate Levels