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A- and F3-Adrenergic Stimulation of Arachidonic Acid Metabolism In Proc. Natl. Acad. Sci. USA Vol. 76, No. 12, pp. 6632-6636, December 1979 Medical Sciences a- and f3-adrenergic stimulation of arachidonic acid metabolism in cells in culture (phospholipase A2/prostaglandins/adrenergic antagonists/norepinephrine/adrenergic receptors) LAWRENCE LEVINE* AND MICHAEL A. MOSKOWITZtt *Department of Biochemistry, Brandeis University, Waltham, Massachusetts 02154; tLaboratory of Neuroendocrine Regulation, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; and *Section of Neurology, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115 Communicated by H. N. Munro, September 12,1979 ABSTRACT Madin-Darby canine kidney cells (MDCK) We now report that the regulation of PG biosynthesis is con- synthesize prostaglandin (PG) F2, PGI2 (measured as 6-keto- trolled, in part, by a- or f3-adrenergic receptors which, when PGEia), PGE2, PGD2, and thromboxane A2 (measured as thromboxane B2). When incubated in the presence of norepi- stimulated, promote the deacylation of phospholipids and nephrine (6 p&M), the syntheses of these arachidonic acid me- subsequent metabolism of arachidonic acid. tabolites are stimulated -fold. Norepinephrine's effect can be antagonized by the addition of a-adrenergic receptor blocking MATERIALS AND METHODS agents (phenoxybenzamine>phentolamine>yohimbine>di- Cell Cultures. Exponentially growing dog kidney (MDCK) benamine>tolazoline) but not by the 0-adrenergic blocking drug propranolol. Norepinephrine's stimulation is also inhibited by cells were treated with 0.25% trypsin and seeded at 2 X 105 cells low concentrations of dihydroergotamine, bromocryptine, er- per 60-mm Falcon tissue culture dish in 4 ml of Eagle's minimal gocryptine, and ergotamine. The stimulation of PG synthesis essential medium containing 2 mM i-glutamate and supple- by norepinephrine is reversible, continues during the 24 hr of mented with 10% (vol/vol) fetal bovine serum, 250 units of incubation, and requires the presence of norepinephrine at the penicillin per ml, and 250 jg of streptomycin per ml; they were receptor site but it is not blocked by the addition of colchicine, incubated for 24 hr. In the experiments described below, the cytochalasin B, or cycloheximide. Neither phenoxybenzamine nor ergotamine at concentrations that block norepinephrine's cells were washed twice with 2 ml of the medium lacking fetal stimulation of PG biosynthesis suppresses the increase in PG bovine serum and incubated with 4 ml of the medium lacking synthesis induced by exogenous arachidonic acid, suggesting the fetal bovine serum but containing the experimental re- that the a-adrenergic regulation is not occurring primarily at agents. the cyclooxygenase step in the metabolism of arachidonic acid. Assay of Arachidonic Acid Metabolites. Thromboxane A2 In mouse lymphoma cells (WEHI-5), low concentrations of as TBXB2), PGE2, and PGD2 were isoproterenol or norepinephrine stimulate the synthesis of (TBXA2) (measured PGF2., thromboxane, an effect that can be blocked by the addition of measured in culture fluids by radioimmunoassay using antisera propranolol but not by relatively high concentrations of whose serologic properties have been described (13, 14). Pros- phenoxybenzamine or ergotamine. Taken together, these results tacyclin, measured as 6-keto-PGF1a, was also measured by suggest that a-adrenergic receptor stimulation promotes the radioimmunoassay. In this system, 10 pg of 6-keto-PGFia in- deacylation of phospholipids by MDCK cells whereas 0- hibited the binding of 6-keto-[3H]PGFia to anti-6-keto-PGFia adrenergic mechanisms lead to activation of similar pathways by 50%; PGE2, PGF2a, and PGA2 crossreacted less than 1%. In in WEHI-5 cells. some experiments, separation and quantitation of arachidonic The mechanism by which catecholamines stimulate the bio- acid metabolites were performed as reported (15). Briefly, synthesis of prostaglandin-like substances in adipose tissue (1, conditioned medium from MDCK cells was first acidified to 2), spleen (3-6), lungs (7), phrenic diaphragm (8,9), brain (10), pH 3.5 and the arachidonic acid metabolites were adsorbed onto kidney (11), and skin (2) is poorly understood. It is possible that XAD-2 resin (ISOLAB, Akron, OH). The resin was washed with these compounds stimulate via receptor-mediated mechanisms; 20 ml of H20, and arachidonic acid metabolites were eluted for example, treatment with the a-adrenergic receptor blocking with 100% ethanol. The eluates were dried under nitrogen at agent phenoxybenzamine inhibits the appearance of prosta- room temperature and resuspended in ethanol. Samples were glandin-like material from dog spleen (3,4, 6) and rabbit kidney then clarified by centrifugation, concentrated by drying under (11) after the administration of norepinephrine (NE). It is also nitrogen, and subjected to high-pressure liquid chromatography possible that prostaglandin-like substances are released as a using a reversed-phase system (15). The eluted fractions were result of tissue contraction (e.g., splenic capsule) induced by the assayed by radioimmunoassay. In other experiments, the con- catecholamines (6). On the other hand, stimulation of prosta- ditioned media were analyzed directly by radioimmuno- glandin (PG) synthesis by the catecholami-nes may simply re- assay. flect their properties as cofactors for the cyclooxygenation of Chemicals. Drugs used in this study were purchased from arachidonic acid, as shown by studies using microsomes pre- Sigma except as noted. The tritiated arachidonic acid metab- pared from seminal vesicles (12). olites were purchased from New England Nuclear. In the present study, we examined the relationship between Stock solutions of a-adrenergic antagonists in dimethyl catecholamine receptors and PG synthesis by cells in culture. sulfoxide were stored in the dark at -20°C. Dilutions were made in medium lacking fetal bovine serum just prior to the The publication costs of this article were defrayed in part by page experiment, and the appropriate amount was added to the charge payment. This article must therefore be hereby marked "ad- vertisement" in accordance with 18 U. S. C. §1734 solely to indicate Abbreviations: NE, norepinephrine; PG, prostaglandin; TBX, this fact. thromboxane. 6632 Downloaded by guest on September 29, 2021 Medical Sciences: Levine and Moskowitz Proc. Natl. Acad. Sci. USA 76 (1979) 6633 culture dish. The highest level of dimethyl sulfoxide used (0.1%) values (unpublished data).] Hence, all subsequent analyses were had no effect on MDCK cells or production of PGs. Solutions performed by radioimmunoassay of the conditioned media of the a- and f3-adrenergic agonists as well as propranolol were without separation, unless otherwise indicated. freshly made for each experiment in the medium lacking fetal NE in doses as low as 2-10 ,tM stimulated the production of bovine serum. None of the reagents at the concentrations used PGE2, PGI2, TBXA2, and PGD2 without affecting the interfered with the radioimmunoassays. numberPGF2.,or viability of cells. When measured after 24 hr of in- cubation, 6 AM norepinephrine stimulated synthesis of all of RESULTS these products 3-fold (Fig. 2). The NE effect continued for at The MDCK cells synthesized PGF2a, PGI2 (measured as 6- least 24 hr but was not inhibited by addition of cycloheximide keto-PGFIa), PGE2, PGD2, and' TBXA2 (measured as TBXB2) (0.2 ,ug/ml), colchicine (1 Mug/ml), or cytochalasin B (0.1 ug/ml) (Fig. 1). In order to maximize arachidonic acid metabolism so and therefore does not depend upon the synthesis of protein or that the metabolic profile could be clearly demonstrated, in the integrity of microtubules or microfilaments. The possibility that experiment shown in Fig. 1 the cells were stimulated to me- NE was inhibiting catabolism of PGE2, PGF2a, TBXA2, PGI2, tabolize polyenoic acids by incubation with a tumor-promoting and PGD2 by 15-hydroxydehydrogenase and A13-reductase was phorbol diester [the phorbol diester stimulates deacylation of unlikely because the metabolites of PGE2 and PGF2a, the cellular lipids (16, 17) and provides the polyenoic substrates 15-keto- and 13,14-dihydro-15-keto derivatives, are not found required for the synthesizing enzymes of PG, TBX, and pros- in MDCK cells or their culture fluids (15). Epinephrine and tacyclin]. Such treatment stimulates PG production 5- to 10-fold dopamine also stimulate PG production. At 10 ,uM, epinephrine (16,'17). Radioimmunoassay of arachidonic acid metabolites was the most potent of the agonists tested; isoproterenol did not before and after separation by high-pressure liquid chroma- stimulate PG production at any of the concentrations tested tography gave similar values. [Radioimmunoassay of condi- (2-20 MM). tioned media from cells established from mouse lymphoma, The effects of NE (6 ,M) could be blocked by addition of low bovine aorta, rabbit aorta smooth muscle, normal human concentrations of the a-adrenergic receptor blocking agents foreskin, normal human embryonic lung, and a rat adult type phenoxybenzamine or ergotamine (Fig. 3). The blockade (like II alveolar cell before and after separation also gave comparable the stimulation by NE) seems to occur at either the cyclooxy- genase or phospholipase reaction because all of the arachidonic acid metabolites were inhibited to a similar extent. To distin- 1000 guish between these two possible loci of activity, PG synthesis was stimulated by incubating the cells in the presence of ara- PGF20f chidonic acid. The arachidonic acid-induced stimulation was not blocked by high concentrations of phenoxybenzamine (3 K 6KFia MM) or ergotamine (0.7 MM) (Table 1). Because it has been 10o shown (17) that little, if any, free arachidonic acid exists in MDCK cells, it seems most likely that NE promotes the deac- 0.7 0.07 0 0.6 _ 0.06 - 1- -0.5 -E 0.05 - C 0, 0 c ._r c' 0.4 ', 0.04 M - 4-(U u 0.3 O/OA X 0.03 PGD2 H- TBXB2 R ' 0.2 0.02 -5 1 0.1 0.01 ) 5 10 15 20 25 0 5 10 15 20 25 6.0 0.1 I _ 5.0 E c , 4.0 0~~~ 6 3.0 U- 6 0 a.
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