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1.
The glucocorticoid dexamethasone (Dex) induces a decline in protein synthesis and protein content in tissue cultured, avlan skeletal muscle cells, and this atrophy is attenuated by repetitive mechanical stretch. Since the prostaglandin synthesis inhibitor indomethacin mitigated this stretch attenuation of muscle atrophy, the effects of Dex and mechanical stretch on prostaglandin production and prostaglandin H synthase (PGHS) activity were examined. In static cultures, 10?8 M Dex reduced PGF2α production 55–65% and PGE2 production 84–90% after 24–72 h of incubation. Repetitive 10% stretch-relaxations of non-Dex-treated cultures increased PGF2α efflux 41% at 24 h and 276% at 72 h, and increased PGE2 production 51% at 24 h and 236% at 72 h. Mechanical stimulation of Dex-treated cultures increased PGF2α production 162% after 24 h, returning PGF2α efflux to the level of non-Dex-treated cultures. At 72 h, stretch increased PGF2α efflux 65% in Dex-treated cultures. Mechanical stimulation of Dex-treated cultures also increased PGE2 production at 24 h, but not at 72 h. Dex reduced PGHS activity in the muscle cultures by 70% after 8–24 h of incubation, and mechanical stimulation of the Dex-treated cultures increased PGHS activity by 98% after 24 h. Repetitive mechanical stimulation attenuates the catabolic effects of Dex on cultured skeletal muscle cells in part by mitigating the Dex-induced declines in PGHS activity and prostaglandin production. © 1994 wiley-Liss, Inc. 相似文献
2.
J.M. Katz S.J.M. Skinner T. Wilson D.H. Gray 《Prostaglandins & other lipid mediators》1983,26(4):545-555
Mouse calvaria were maintained in organ culture without serum additives. Basal active resorption, as measured by 45Ca and hydroxyproline release, was significantly inhibited to 74% control levels by indomethacin (1.4 × 10−7 M). Prostaglandin F and prostaglandin E2 production, determined by radioimmunoassay, were both significantly lowered by this concentration of indomethacin. DNA, protein and hydroxyproline synthesis, as indices of cell toxicity, were unaffected by low concentrations of indomethacin, while concentrations of 1.4 × 10−6M inhibited protein synthesis (p<0.005). In the presence of indomethacin (1.4 × 10−7M) both PGE2 and PGF2α stimulated resorption in a dose-dependent manner, with PGE2 being the more potent. Neither prostaglandin affected hydroxyproline synthesis at low concentrations, but PGE2 had a marked inhibitory action at a higher concentration (10−6M). In combination, the effects of PGE2 and PGF2α showed no evidence of synergism or any antagonistic action. The study shows that in vitro calcium and hydroxyproline resorption in the unstimulated mouse calvaria are inhibited by indomethacin at concentrations measured in serum during human therapy. The decreased PGF and PGE2 production associated with this decreased bone resorption in the presence of non-toxic concentrations of indomethacin would suggest a role for these prostaglandins in maintaining the basal resorption of cultured bone. 相似文献
3.
《Cell biology international reports》1982,6(10):961-967
Retinoic acid at concentrations of 10−8–10−6M increases the initiation of DNA synthesis stimulated by prostaglandin F2α (PGF2α), alone or with insulin, in confluent resting Swiss mouse 3T3 cells. Analogues of retinoic acid had a similar effect. Adding retinoic acid, alone or with insulin, did not stimulate DNA synthesis. The synergistic effect of PGE1 or PGE2 with PGF2α and insulin was not further enhanced by retinoic acid. Neither the synergistic effect of retinoic acid nor that of PGE1 or PGE2 with PGF2α was affected by indomethacin, an inhibitor of prostaglandin synthesis. The results suggest that the synergy of retinoic acid with PGF2α is not mediated through an increase of prostaglandin synthesis and that retinoic acid stimulates event(s) in common with those of PGE1 and PGE2 leading to an increase in the initiation of DNA synthesis. 相似文献
4.
D. J. Orlicky M. Silio C. Williams J. Gordon L. E. Gerschenson 《Journal of cellular physiology》1986,128(1):105-112
Stimulation of cultured rabbit endometrial cells by one of the rabbit endometrial cell culture proliferation factors, prostaglandin F2α (PGF2α), resulted in a very rapid increase in the intracellular levels of [3H]-inositol triphosphate (IP3), [3H]-inositol biphosphate (IP2), and [3H]-inositol monophosphate (IP1) in cells prelabeled with [3H]-inositol. These increases in inositol phosphate levels were detected in periods of stimulation as short as 30 seconds, reached a maximum by 1 1/2?2 min and declined to control levels by 6–10 min. The stimulation was dose-dependent with maximal increases observed near 10?6 M PGF2α. The cholinergic agent, carbachol, also led to time and dose-independent increases in IP3. Lithium, cadmium, silver, copper, and zinc ions had no effect either on the breakdown of IP3 or on the accumulation of IP1. In contrast, vanadate at 10?6 or 10?5 M did lead to a decrease in the breakdown of IP1 and a concomitant increase in IP1, IP2, and IP3. PGF2α was found previously to induce an increase in rabbit endometrial cell DNA synthesis which was inhibited by concomitant or prior addition of prostaglandin E1 (PGE1). PGE1, in a dose-dependent manner, was found to inhibit the observed IP3 increase by PGF2α at 1 1/2 min of stimulation. PGF2α treated and control cultures did not differ in cAMP or cGMP levels, cellular 45Ca uptake, nor cellular 22Na uptake. We propose that IP3 may be one of the intracellular messenger(s) synthesized following the treatment of rabbit endometrial cell cultures with the proliferation agent PGF2α and that it may play a crucial role with cAMP in growth regulation. 相似文献
5.
Synthetic leukotrienes (LT) C4 and D4 elicited concentration-dependent contractions of the guinea pig uterus between 10?8-10?6M, whereas LTE4 appeared 1000-fold weaker. The potencies of LTC4 and LTD4 were similar to that of acetylcholine and PGF2α but weaker than that of PGE2. The maximal contractions elicited by LTC4 and LTD4 were 66.0 ± 2.1% and 63.8 ± 4.6% that elicited by acetylcholine. FPL 55712 (10?5M) antagonized the uterine contractile activity of LTD4, while meclofenamic acid at 10?5M but not at 10?6M also antagonized the LTD4-induced contration. Radioimmunoassay of the uterine tissue bathing fluid following LTD4 indicated the variable presence of low concentrations of PGE2, PGF2α and TXB2. These results demonstrate the LTC4 and LTD4 possess significant uterine contractile activity, which may only partially be mediated indirectly via prostaglandin products. 相似文献
6.
Philippe Leroux Marie-Christine Tonon Sylvie Jégou Catherine Delarue François Leboulenger Pierre Netchitaílo Hubert Vaudry 《Prostaglandins & other lipid mediators》1981,21(4):599-608
A possible direct effect of prostaglandins on α-melanotropin (α-MSH) release at the level of the intermediate lobe of the frog pituitary was investigated using a perifusion system technique. The effect of prostaglandins was studied on both spontaneous and TRH-stimulated α-MSH secretion. No significant effect of PGE1, PGE2, PGF1α or PGF2α on basal release of α-MSH could be detected. Indomethacin did not alter the α-MSH release induced by TRH. Conversely a significant increase in TRH-induced α-MSH secretion was observed in the presence of 1 x 10?6M PGE1. This magnifying effect was directly related to the concentration of TRH for doses ranging from 1 x 10?8M to 1 x 10?6M. 相似文献
7.
C V Rao 《Biochemical and biophysical research communications》1975,64(1):416-424
The cell membranes isolated from bovine corpora lutea bound 3H-prostaglandin (PG) F2α with high affinity and specificity. The specific binding of 3H-PGF2α was detectable at 10?10M added 3H-PGF2α and reached saturation at 10?7M to 10?6M. Unlabeled PGF2α, as low as 10?9M, inhibited the binding of 3H-PGF2α with complete inhibition occurring at 10?6M. The Scatchard analysis of equilibrium binding data revealed that the PGF2α receptors are heterogeneous: Kd1?5.1 × 10?9M, n?289 fmoles/mg protein; Kd2?1.8 × 10?8M, n?780 fmoles/mg protein. The relative affinities of various other PGs for binding to PGF2α receptors were (PGF2α?100%): PGF1α?17.5; PGE1?0.8; PGE2?22.4; PGA1?0.007; PGB1?0.01. The specificity and affinity of 3H-PGF2α binding is consistent with the possibility that this receptor interaction may reflect an initial event in the action of PGF2α as a luteolytic agent. 相似文献
8.
Production of prostaglandins by cells in vitro: radioimmunoassay measurement of the conversion of arachidonic acid to PGE2 and PGF2 alpha 总被引:3,自引:0,他引:3
A specific radioimmunoassay has been applied to the measurement of the conversion of arachidonic acid to PGE2 and PGF2α. PGE2 and PGF2α biosynthesis was linearly related to the amount of arachidonic acid added and was significantly inhibited by indomethacin in concentrations as low as 10?10 M. Sonicated Hela, L, and HEp-2 cells synthesized 244.0, 42.3, and 22.6 ng PGE2 per mg of protein, but made substantially less PGF2α. 相似文献
9.
We have tested the action of a catechol oestrogen -2,3,17β- trihydroxy oestra-1,3,5 (10)-triene (2-OH oestradiol) in stimulating prostaglandin (PG) production by an homogenate of rat uterus. Marked and dose dependent stimulation was observed in PGF2α and PGE2 production using 20–250 μM concentrations of catechol oestrogen; a concentration of 250 μM 2-OH oestradiol resulted in a 23 fold increase in PGF2α production with a 50% reduction in the synthesis of 6-keto PGF1α. Tryptophan, catechol and glutathione were without effect on PGF2α and PGE2 production whereas adrenalin stimulated the production of all PGs, although the increase was less than that seen with 2-OH oestradiol. Oestradiol had a slight stimulatory action on PGF2α production which reached a maximum at around 40 μM but had a more marked stimulation of 6-keto PGF1α formation. Stimulation of prostaglandin production by oestradiol and 2-OH oestradiol showed no variation at different stages of the rat oestrous cycle. The use of 5 to 100 mg of tissue/ml gave similar product distribution although the effect of catechol oestrogen both in terms of stimulation of E and F formation (expressed per mg of tissue) and in its action on product distribution was more marked at lower concentrations of tissue. 相似文献
10.
Epidermal growth factor stimulates prostaglandin production and bone resorption in cultured mouse calvaria. 总被引:6,自引:0,他引:6
Murine epidermal growth factor (EGF) stimulated the production of prostaglandin E2 (PGE2) and bone resorption in neonatal mouse calvaria in organ culture. The effect of EGF on bone resorption occurred at low concentrations of the polypeptide (half-max stimulation = 0.4 ng/ml, 6.6 × 10?11 M). All concentrations of EGF which stimulated resorption also stimulated the production of PGE2 by bone; concentrations of EGF which did not stimulate resorption did not enhance PGE2 production. EGF-induced formation of PGE2 and bone resorption were inhibited completely by indomethacin (200 ng/ml) and hydrocortisone (3 × 10?6 M). Indomethacin did not inhibit the bone resorption-stimulating activity of exogenous PGE2. The time courses of action of EGF, parathyroid hormone and exogenous PGE2 on bone resorption were similar. Brief exposure (15 or 60 min) to EGF (10 ng/ml) did not cause bone resorption or an increase in PGE2 accumulation in a subsequent 48-h incubation in the absence of EGF. High concentrations (30 to 100 ng/ml) of bovine fibroblast growth factor (FGF) also stimulated the production of PGE2 and bone resorption. We conclude that concentrations of EGF equal to or less than those present in mouse plasma stimulate the resorption of mouse bone in organ culture by a mechanism that involves the enhanced local production of PGE2. 相似文献
11.
Cyclic AMP production by freshly isolated cells, from a 32P-induced transplantable rat osteogenic sarcoma, was stimulated by PGE1, PGE2 and to a less extent by PGF2α and PGA2. In the case of PGE2, the cyclic AMP content of cells was miximal within 5 min. The 13, 14-dihydro derivatives of PGE1, PGE2 and PGF2α had approximately 40% of the activity of the parent prostaglandin whilst, in every case, the metabolites (15-keto and 13,14-dihydro-15-keto) had very little activity. Two prostaglandin endoperoxide analogues (U44069 and U46619) had only 10% of the activity of an equimolar dose of PGE2. The data presented in this paper demonstrates similarities between the responses of these cells and cells derived from bony tissue in terms of the ability of prostaglandins to stimulate bone resorption in tissue culture. 相似文献
12.
Prostaglandins (PG) of both the E and F series may serve as modulators of norepinephrine (NE) release from peripheral sympathetic neurons. We have studied the effects of PGE2 and PGF2α on the accumulation and release of 3H-NE in the CNS using synaptosomes isolated from rat hypothalami.The release of 3H-NE from synaptosomes superfused with Krebs-Ringer bicarbonate buffer was multiphasic with an initial fast release phase followed by a slower release. Raising KC1 concentration of the superfusion medium to 56mM during the slow release phase is known to stimulate 3H-NE release. PGE2 (1 × 10?6M) attenuated 3H-NE release during the fast phase and reduced the amount of 3H-NE released due to KC1 stimulation. At lower concentrations of PGE2 there was no change in the release profile. PGF2α was without effect on 3H-NE release at all concentrations tested.The accumulation of 3H-NE was significantly diminished by PGE2 at a concentration of 1 × 10?6M, while a lower concentration (1 × 10?7M) was ineffective. PGF2α had no effect on 3H-NE accumulation at all concentrations investigated. 相似文献
13.
Ch.V. Rao 《Prostaglandins & other lipid mediators》1973,4(4):567-576
The cell membranes exhibited specific binding to 3H-prostaglandin E1 (3H-PGE1) and 125I-human chorionic gonadotropin (125I-HCG). Unlabeled PGE1,PGE2 (1.4 × 10?7M), PGF1α and PGF2α (1.4 × 10?5M) decreased 3H-PGE1 binding by more than 80%. The binding of 125I-HCG was completely inhibited by 5 × 10?8M unlabeled HCG. However, the unlabeled PGE1 (1.15 × 10?6M) and HCG (8.4 × 10?7M) had no effect on 125I-HCG and 3H-PGE1 binding respectively. A PG antagonist, 7-oxa-13-prostynoic acid, inhibited only 3H-PGE1 binding but not 125I-HCG binding. These results suggest the presence of specific receptors for PGE1 and HCG in the cell membranes and that the binding occurs either at two different sites on the same receptor or that each binds to a “different” receptor molecule. 相似文献
14.
M Lahav A Freud H R Lindner 《Biochemical and biophysical research communications》1976,68(4):1294-1300
Corpora lutea explanted from rats on the sixth day of pregnancy responded to luteinizing hormone (LH; 5 μg/ml) in vitro with a two- to five-fold increase in cellular cyclic AMP (cAMP) concentration. The maximal cAMP level was reached within 60 min and maintained to the end of the 2 hr-incubation. On incubation with prostaglandin F2α (PGF2α) in addition to LH, this rise in cAMP accumulation was prevented. For significant suppression, 1.4 × 10?5M PGF2α was required. In the absence of LH, PGF2α (4.2 × 10?5M) caused no change in cellular cAMP. Addition of PGF2α (4.2 × 10?5M) to the incubation medium after the maximal response to LH was attained, caused the cAMP concentration to return to its basal level within 15 min. This abrogation of LH-stimulated cAMP accumulation represents the earliest and hence possibly the triggering event in PGF2α-induced luteolysis. 相似文献
15.
《Prostaglandins, Leukotrienes and Medicine》1986,21(1):15-22
While no significant effects on the in vitro production of PGF2α by homogenates of rat estrous uteri were observed in the presence of 10−3 and 10−6M Cu2+, the presence of Cu2+ at 10−4 and 10−5M was found to stimulate production with maximal synthesis of PGF2α occurring with 10−4M Cu2+. By contrast, the synthesis of PGE2 and PGI2 (determined as 6-keto PGF1α) were unaffected at all of the different Cu2+ concentrations used. When indomethacin and salicylic acid were tested for their effects on the Cu2+-mediated levels of PG synthesis by the homogenates, indomethacin (at 20μM) was found to cause similar pronounced decreases in PGF2α, PGE2 and 6-keto PGF1α whereas salicylic acid (400μM) showed preference towards suppressing PGE2 and 6-keto PGF1α production. 相似文献
16.
Intact viable bovine luteal cell suspensions prepared by collagenase digestion of luteal tissue were used in studying the selected properties of [3H] prostaglandin (PG) F2α binding and compared with those observed in plasma membranes. [3H]PGF2α specific binding to luteal cells was a rapid (K1 = 8.4 × 104M?12αS?1), reversible (K?1 = 1.8 × 10?4S?1) and saturable process at 24°. There was a single class of receptors with an apparent dissociation constant of 10.6 nM and 1.8 × 105 receptors per cell. The presence of increasing amounts of unlabeled PGs inhibited [3H]PGF2α binding in a dose-dependent manner. The potency order for this inhibition was: (15S) 15-methyl-PGF2α methyl ester > ICI-80,996 > PGF2α > ICI-81,008 > PGF1α > PGE2, (15S) 15-methyl-PGE2 methyl ester > PGF2α metabolites > other PGs, PGF1α metabolites and PGE metabolites. Other than the homegeneous nature of binding and a greater association rate in cells, the rest of the [3H]PGF2α binding properties in cells were in good agreement with those observed in plasma membranes. 相似文献
17.
Bovine articular chondrocytes, cultured as cell suspensions and monolayers, produced prostaglandin (PG) E2 and PGI2 (assayed as 6 keto PGF1α), rather less PGF2α and irregular quantities of thromboxane (Tx) B2. Addition of foetal calf serum to the medium greatly stimulated PG production (a sixfold increase in PGE2 and a twofold increase in 6 keto PGF1α).Prostanoid production by cell suspension grown in serum-free medium generally plateaued after 24 hours. In the presence of 20% foetal calf serum, prostanoid production in long-term monolayer cultures increased during the first 6 days of culture. Levels of PGE2α levels remained high. Indomethacin (10-6M) inhibited chondrocyte PG production both in the presence and absence of added arachidonic acid (10-4M). Prostanoids produced by chondrocytes may play a role in the modulation of cartilage metabolism . 相似文献
18.
The response of endothelial adenylate cyclase (AC) to prostaglandins (PGE1, PGE2, PGF1α, PGF2α, PGD2 and PGI2) and the relationship of PGE2 to adrenergic systems were investigated in cerebrovascular endothelial cultures. E-type prostaglandins and PGI2 were more effective in stimulating endothelial AC (EC50 = 3 × 10?7M, and 3 × 10?7M, respectively) than prostaglandins of the F-series and PGD2 which activated AC at high doses only. A modulation of endothelial AC response to either PGE2 or norepinephrine (NE) was observed in the presence of both agents in the system. It was manifested by a dose-dependent NE inhibition of the PGE2-stimulated formation of cAMP, which was partially restored by phentolamine. Alpha and β-adrenergic agonists (α, clonidine and 6-fluoronorepinephrine; β, isoproterenol) also partly blocked while forskolin and PGE2 synergistically stimulated the production of cAMP in the endothelial cultures. These findings strongly suggest that the interaction of prostaglandins and α- and β-adrenergic agonists with the AC system in cerebrovascular endothelium may play a role in the regulation of the cerebral microcirculation and/or blood pressure. 相似文献
19.
R. K. Kowalski K. Shiba M. Yoshida J. Glogowski 《Zeitschrift fur angewandte Ichthyologie》2008,24(4):487-491
The purpose of this study was to determine the concentrations of prostaglandins E2 and F2α (PGE2 and PGF2α) in the blood, testis and seminal plasma of mature male rainbow trout and in the ovarian fluid to assess the effects of these prostaglandins on sperm motility parameters when present in activation media. Also prolonged incubation with prostaglandins on sperm motility and calcium influx were studied. The profile of PGE2 and PGF2α differed in concentration between blood, testicular supernatant and seminal plasma. PGE2 was predominant in the blood sample (0.29 ng ml?1) and testicular supernatant (3.1 ng ml?1) whereas their level in seminal plasma was lower than PGF2α (0.23 ng ml?1). The concentrations of PGF2α in blood, testis and seminal plasma were 0.04, 0.99, 1.3 ng ml?1, respectively. In the ovarian fluid the concentrations of both prostaglandins were higher than in the male reproductive tract. Adding both prostaglandins to activation buffer (at concentrations 15 and 70 ng ml?1) had no effect on any CASA parameters. Calcium influx related to rainbow trout sperm incubations with PGE2, and PGF2α was not detected. After 24 h incubation of sperm in artificial seminal plasma solution without and with prostaglandins all sperm samples increased their motility potential and intracellular calcium concentration. Therefore, this effect was not related to the presence of prostaglandins. In summary PGE2, and PGF2α were present in the rainbow trout male reproductive tract, and their profile varies from that of blood, testis and seminal plasma. The specific role of both prostaglandins in salmonid sperm biology remains unclear. 相似文献
20.
S.C. Hung N.I. Ghali D.L. Venton G.C. Le Breton 《Prostaglandins & other lipid mediators》1982,24(2):195-206
The effects of prostaglandin F2α on human blood platelet function were investigated. PGF2α at 15 μM completely blocked platelet aggregation induced by 500 μM arachidonic acid or 3 μM U46619 but had no effect on aggregatin induced by 7.5 μM ADP. A similar specificity of action was not obtained with either PGI2 or PGE2. Thus concentrations of PGI2 (3 nM) or PGE2 (20 μ M) which inhibited U46619-induced aggregation by 100% also blocked ADP-stimulated aggregation.The inhibitory properties of PGF2α were not related to increases in platelet cAMP, since direct measurement of intracellular cAMP revealed that 15 μ M PGF2α produced no substantial change in cAMP levels. This finding was in direct contrast to results obtained using either PGI2 or PGE2. Both PGI2 (3 nM) and PGE2 (20 μ M) induced significant increases in platelet cAMP levels.The possibility that PGF2α directly interacts at the platelet TXA2/PGH2 receptor was investigated by measuring [3H]PGF2α binding to isolated platelet membranes. It was found that [3H] PGF2α binding reached equilibrium within 30 min at room temperature and could be 90% displaced by addition of 1000 fold excess of unlabelled PGF2α. Furthermore, when 1000 fold excess of either the TXA2/PGH2 “mimetic” U46619 or the TXA2/PGH2 antagonist 13-azaprostanoic acid was added, specific [3H] PGF2α binding was displaced by 95% and 85% respectively. In contrast, the same molar excess of 6-keto-PGF1α, azo analog 1, or TXB2, caused displacement of only 15%, 20% or 25% of the [3H] PGF2α binding. Scatchard analysis indicated that [3H] PGF2α has two binding sites; i.e., a high affinity binding site with an apparent Kd of 50 nM and a low affinity binding site with apparent Kd of 320 nM. These results suggest that the selective inhibition by PGF2α of AA or U46619-induced aggregation may be mediated through interaction at the platelet TXA2/PGH2 receptor. 相似文献