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Regulation of COX-2 gene expression in rat uterus in vivo and in vitro COX-2基因在体内外大鼠子宫中的表达调控
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(96)00125-6
Ali Arslan, Hans H. Zingg
{"title":"Regulation of COX-2 gene expression in rat uterus in vivo and in vitro","authors":"Ali Arslan,&nbsp;Hans H. Zingg","doi":"10.1016/S0090-6980(96)00125-6","DOIUrl":"10.1016/S0090-6980(96)00125-6","url":null,"abstract":"<div><p>Prostaglandins are involved in mediating several important processes in mammalian reproduction, including the initiation of parturition. In the present study, we examined the expression in the rat uterus of two-rate limiting enzymes involved in prostaglandin production, cyclooxygenase (COX) 1 and 2. Expression of the COX-2 gene in the pregnant rat uterus gave rise to a single mRNA transcript of approximately 4.4 kb. COX-2 mRNA levels increased 3.5 fold between day 7 of pregnancy and the onset of parturition on day 22. In contrast, COX-1 mRNA levels remained constant during the same period. To investigate factors involved in mediating the regulation of COX-1 and COX-2 gene expression, rat endometrial stromal and epithelial cell lines, were used. In the stroma-derived cell line, CUS-V2, COX-2 gene expression was demonstrated by reverse transcriptase/polymerase chain reaction (RT-PCR) and by immunocytochemistry. In these cells, COX-2 gene expression was inducible by the cytokines interleukin-1 β and tumor necrosis factor α, but not by interleukin-6. The two former cytokines also induced prostaglandin F<sub>2α</sub> production. In contrast, COX-1 gene expression was constitutive in this cell line. In the endometrial epithelium-derived cell line, CUE-P both COX-1 and COX-2 genes were expressed in a constitutive fashion. In conclusion, the present in vivo and in vitro data indicate that decidual COX-2, but not COX-1, gene expression is regulated during pregnancy and implicate specific cytokines as possible inducers within the decidua.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00125-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19940060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 60
Author index volume 52 July–December 作者索引卷52 7 - 12月
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(97)82244-7
{"title":"Author index volume 52 July–December","authors":"","doi":"10.1016/S0090-6980(97)82244-7","DOIUrl":"https://doi.org/10.1016/S0090-6980(97)82244-7","url":null,"abstract":"","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)82244-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137205562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cysteinyl leukotrienes do not mediate lipopolysaccharide-induced airway hyperresponsiveness in guinea pigs 半胱氨酸白三烯不介导豚鼠脂多糖诱导的气道高反应性
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(96)00126-8
Takashi Uno, Hiroyuki Tanaka, Hiroichi Nagai
{"title":"Cysteinyl leukotrienes do not mediate lipopolysaccharide-induced airway hyperresponsiveness in guinea pigs","authors":"Takashi Uno,&nbsp;Hiroyuki Tanaka,&nbsp;Hiroichi Nagai","doi":"10.1016/S0090-6980(96)00126-8","DOIUrl":"10.1016/S0090-6980(96)00126-8","url":null,"abstract":"<div><p>Inhalation of bacterial lipopolysaccharide (LPS) by guinea pigs caused bronchial hyperreactivity to acetylcholine with a peak at 2 hr after exposure. Exposure to 0.01% LPS for 30 min resulted in an elevation of cysteinyl leukotrienes (cys-LTs) content in bronchoalveolar lavage fluid (BALF) which was obtained 1 hr after LPS exposure. The cys-LTs antagonist, ONO-1078 (10 mg/kg, p.o.), significantly inhibited LPS-induced bronchial hyperreactivity, but ICI-204,219 (10 mg/kg, p.o.), another cys-LT antagonist, did not. Each dose employed in the present study was sufficient to inhibit LTD<sub>4</sub> induced broncho-constriction in guinea pigs. In order to investigate the inhibitory mechanism of ONO-1078, the effect on the LPS-induced production of tumor necrosis factor (TNF) was examined. The amount of TNF in BALF increased significantly 2 hr after exposure to LPS. The inhalation of murine recombinant TNF-α (5 × 10<sup>4</sup> u/ml) resulted in bronchial hyperreactivity in guinea pigs. ONO-1078 (10mg/kg, p.o.) inhibited the increase of LPS-induced TNF in BALF, but ICI-204,219 (10 mg/kg, p.o.) had no effect. These results suggest that TNF plays an important role in the onset of LPS-induced bronchial hyper-reactivity, and that ONO-1078 inhibits the LPS-induced airway hyperreactivity probably due to the inhibition of TNF production.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00126-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19940059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
Interaction between nitric oxide and prostaglandin synthesis in the acute phase of allergic conjunctivitis 过敏性结膜炎急性期一氧化氮与前列腺素合成的相互作用
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(96)00123-2
F. Meijer , C. Tak , N.J. van Haeringen , A. Kijlstra
{"title":"Interaction between nitric oxide and prostaglandin synthesis in the acute phase of allergic conjunctivitis","authors":"F. Meijer ,&nbsp;C. Tak ,&nbsp;N.J. van Haeringen ,&nbsp;A. Kijlstra","doi":"10.1016/S0090-6980(96)00123-2","DOIUrl":"10.1016/S0090-6980(96)00123-2","url":null,"abstract":"<div><p>Both nitric oxide and prostaglandins induce vasodilatation which is an important feature of local inflammation. The purpose of the study described here was to investigate a possible interaction between these two types of mediators in an experimental model of allergic conjunctivitis. A conjunctival allergic reaction was induced with antigen in sensitized guinea pigs. Conjunctival vascular permeability changes were evaluated with the prophylactic use of an inhibitor of nitric oxide synthase (L-NAME) and a cycloxygenase inhibitor (indomethacin). To study a possible interaction between nitric oxide and prostaglandin synthesis in the acute phase of allergic conjunctivitis, the levels of nitrite and PGE<sub>2</sub> were determined in lavage fluid. The prophylactic use of L-NAME on the formation of conjunctival edema in response to topical PGD<sub>2</sub> administration was studied by measurement of albumin levels in lavage fluid. Both nitric oxide and PGE<sub>2</sub> are synthesized in response to antigen provocation and after histamine administration. Nitric oxide and PGE<sub>2</sub> are produced simultaneously in the conjunctiva and they showed identical synthesis profiles in response to antigen provocation. Pretreatment with L-NAME inhibited the synthesis of PGE<sub>2</sub> whereas exogenous administration of nitric oxide increased the level of PGE<sub>2</sub> in lavage fluid. Prophylactic treatment with L-NAME significantly inhibited the PGD<sub>2</sub> induced albumin extravasation. Nitric oxide seems to play an important role in the acute phase of allergic conjunctivitis it may stimulate PGE<sub>2</sub> production and acts as a secondary mediator in PGD<sub>2</sub> and histamine induced conjunctival edema.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00123-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19940058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 19
Subject index volume 52 July–December 主题索引卷52 7 - 12月
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(97)82245-9
{"title":"Subject index volume 52 July–December","authors":"","doi":"10.1016/S0090-6980(97)82245-9","DOIUrl":"https://doi.org/10.1016/S0090-6980(97)82245-9","url":null,"abstract":"","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(97)82245-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137205563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Thromboxane A2 analogue contracts predominantly the hepatic veins in isolated canine liver 血栓素A2类似物在离体犬肝脏中主要收缩肝静脉
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(96)00124-4
H. Urayama, T. Shibamoto, H.-G. Wang, S. Koyama
{"title":"Thromboxane A2 analogue contracts predominantly the hepatic veins in isolated canine liver","authors":"H. Urayama,&nbsp;T. Shibamoto,&nbsp;H.-G. Wang,&nbsp;S. Koyama","doi":"10.1016/S0090-6980(96)00124-4","DOIUrl":"10.1016/S0090-6980(96)00124-4","url":null,"abstract":"<div><p>Thromboxane A<sub>2</sub> (TxA<sub>2</sub>) is a potent vasoconstrictor and has been implicated as a mediator of liver diseases such as ischemic-reperfusion injury. We determined the effects of TxA<sub>2</sub> and the well-known hepatic venoconstrictor histamine, on the vascular resistance distribution and liver weight in isolated canine livers perfused with blood via the portal vein. The stable TxA<sub>2</sub> (STA<sub>2</sub>; 20 μg, n=5) and histamine (5 μg, n=6) similarly increased the hepatic total vascular resistance, 2.5- and 2.4-fold, respectively. The increase in the hepatic venous resistance was significantly greater than that of the portal resistance (threefold vs. 1.9-fold for STA2; threefold vs. 1.8-fold for histamine). Predominant hepatic venoconstriction induced by both agents was confirmed in livers perfused in a reverse direction from the hepatic vein to the portal vein, as shown by marked precapillary vasoconstriction. STA2 transiently increased liver weight loss (−3.6 g/100g liver weight), followed by a gradual weight gain (9.0 g/100 g). Histamine caused a progressive weight gain (9.1 g/100 g). In conclusion, similar to histamine, TxA<sub>2</sub> constricts predominantly the hepatic vein in isolated canine livers.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00124-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19940061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 22
Differential effects of indomethacin on the sheep ovary: Prostaglandin biosynthesis, intracellular calcium, apoptosis, and ovulation 吲哚美辛对绵羊卵巢的不同影响:前列腺素生物合成、细胞内钙、细胞凋亡和排卵
Prostaglandins Pub Date : 1996-12-01 DOI: 10.1016/S0090-6980(96)00127-X
W.J. Murdoch
{"title":"Differential effects of indomethacin on the sheep ovary: Prostaglandin biosynthesis, intracellular calcium, apoptosis, and ovulation","authors":"W.J. Murdoch","doi":"10.1016/S0090-6980(96)00127-X","DOIUrl":"10.1016/S0090-6980(96)00127-X","url":null,"abstract":"<div><p>Cells of the apical wall of the dominant follicle and contiguous ovarian surface epithelium become apoptotic with the approach of ovulation in the sheep. It was hypothesized that indomethacin, an established inhibitor of prostaglandin biosynthesis and ovulation, would protect apical ovarian cells from programmed death. The anovulatory potencies of two systemic doses of indomethacin (200 and 800 mg) were tested in gonadotropin-stimulated ewes. A complete blockade of ovulation occurred at the higher dose of indomethacin. Ovulation was not inhibited by 200 mg indomethacin. Both doses of drug suppressed follicular prostaglandin production below pregonadotropin levels. Immunofluorescence detection of digoxigenin end-labeled (fragmented) DNA was used as a marker of apoptosis among ovarian surface epithelial and granulosa cells recovered from the apical hemisphere of preovulatory ovine follicles. Cellular DNA fragmentation was averted in animals given 800 mg indomethacin, whereas apoptosis ensued after 200 mg. A sustained increase in cytosolic calcium is generally a prerequisite to apoptotic DNA fragmentation and cell death. Indeed, intracellular calcium, detected by fluorescence of fura-2, was elevated in ovarian cells of animals destined to ovulate (controls, 200 mg indomethacin) in comparison to (safeguarded) cells of anovulatory ewes (800 mg indomethacin). These observations provide circumstantial evidence that apical ovarian cell degeneration by calcium-mediated apoptosis is a determinant of follicular instability and rupture, but that these events are unrelated to the gonadotropin-induced rise in prostanoid production characteristic of preovulatory follicles.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00127-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19940062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 27
Thromboxane A2 stimulates mitogen activated protein kinase and arachidonic acid liberation in rabbit platelets 血栓素A2刺激有丝分裂原活化蛋白激酶和兔血小板中花生四烯酸的释放
Prostaglandins Pub Date : 1996-11-01 DOI: 10.1016/S0090-6980(96)00105-0
Satoko Ohkubo, Norimichi Nakahata, Yasushi Ohizumi
{"title":"Thromboxane A2 stimulates mitogen activated protein kinase and arachidonic acid liberation in rabbit platelets","authors":"Satoko Ohkubo,&nbsp;Norimichi Nakahata,&nbsp;Yasushi Ohizumi","doi":"10.1016/S0090-6980(96)00105-0","DOIUrl":"10.1016/S0090-6980(96)00105-0","url":null,"abstract":"<div><p>U46619, a thromboxane A<sub>2</sub> mimetic, caused tyrosine phosphorylation of several proteins in rabbit platelets. Among them, 42 kDa protein was identified as a mitogen-activated protein kinase (MAPK). U46619 activated MAPK in a concentration-dependent manner, measured by incorporation of <sup>32</sup>P to a specific substrate for MAPK. U46619 also liberated [<sup>3</sup>H)arachidonic acid in a concentration-dependent manner. The U46619-induced MAPK activation and [<sup>3</sup>H]arachidonic acid liberation were inhibited by SQ29548 and by the removal of external Ca<sup>2+</sup> ions. This is a first demonstration that TXA<sub>2</sub> activates MAPK accompanied with arachidonic acid liberation in rabbit platelets.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00105-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19911960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 30
Constitutive expression of prostaglandin endoperoxide G/H synthetase (PGHS)-2 but not PGHS-1 in hum an tracheal epithelial cells in vitro 前列腺素内过氧化物G/H合成酶(PGHS)-2在肺和气管上皮细胞的组成性表达而非PGHS-1
Prostaglandins Pub Date : 1996-11-01 DOI: 10.1016/S0090-6980(96)00101-3
Ronald W. Walenga Ph.D., Mark Kester Ph.D. , Emanuel Coroneos M.D. , Sarah Butcher, Rohit Dwivedi, Christopher Statt
{"title":"Constitutive expression of prostaglandin endoperoxide G/H synthetase (PGHS)-2 but not PGHS-1 in hum an tracheal epithelial cells in vitro","authors":"Ronald W. Walenga Ph.D.,&nbsp;Mark Kester Ph.D. ,&nbsp;Emanuel Coroneos M.D. ,&nbsp;Sarah Butcher,&nbsp;Rohit Dwivedi,&nbsp;Christopher Statt","doi":"10.1016/S0090-6980(96)00101-3","DOIUrl":"10.1016/S0090-6980(96)00101-3","url":null,"abstract":"<div><p>Primary cultures of human tracheal epithelial (HTE) cells cultured <em>in vitro</em>, in defined serum-free media, express prostaglandin endoperoxide G/H synthase (PGHS) activity and produce prostaglandin E<sub>2</sub> (PGE<sub>2</sub>). In contrast to every other cell type studied to date, HTE cells appear to constitutively express PGHS-2, the ‘inducible’ form of the enzyme, while expressing little or no PGHS-1, the ‘housekeeping’ isoenzyme in vitro. Prostaglandin synthesis in HTE cells was reduced by a selective PGHS-2 inhibitor, N-(2-cyclohexyloyl-4-nitrophenyl] methane-sulfonamide (NS398), with an IC<sub>50</sub> of approximately 1 μM. Immunoblotting and immunoprecipitation of enzymatic activity with isozyme-specific antisera revealed only the PGHS-2 isoform. Full length human cDNA probes detected only PGHS-2 message in Northern blots. Neither PGHS-2 activity nor mRNA levels were dependent on, nor stimulated by peptide growth factors present in the defined serum-free growth medium, or by serum. Prolonged maintenance in the absence of retinoic acid, however, lead to a decline in PGHS activity. Phorbol-myristate acetate (PMA) induced PGHS-2 activity and mRNA and neither PMA-induced, nor constitutive PGHS-2 expression was suppressed by corticosteroids. Actinomycin D-treatment for six hours reduced the PGHS-2 activity and mRNA to only 50% that of untreated cells, suggesting that PGHS-2 mRNA is extremely stable in these cells. HTE cells, at least <em>in vitro</em>, appear unique among prostaglandin-producing cells in that they express PGHS-2, constitutively, independent of regulation by growth factors, serum, or corticosteroids and fail to express PGHS-1 under any culture condition studied.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00101-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19912045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 58
Mechanism of action of TNF-α-stimulated prostaglandin production in cultured bovine luteal cells TNF-α-刺激培养牛黄体细胞前列腺素生成的作用机制
Prostaglandins Pub Date : 1996-11-01 DOI: 10.1016/S0090-6980(96)00104-9
David H Townson, Joy L Pate
{"title":"Mechanism of action of TNF-α-stimulated prostaglandin production in cultured bovine luteal cells","authors":"David H Townson,&nbsp;Joy L Pate","doi":"10.1016/S0090-6980(96)00104-9","DOIUrl":"10.1016/S0090-6980(96)00104-9","url":null,"abstract":"<div><p>Tumor necrosis factor-alpha (TNF-α) influences hormone synthesis of many ovarian cell types and can also exert cytotoxic effects, possibly by increasing the synthesis of prostaglandins. The purpose of the present study was to characterize the mechanism of TNF-α-stimulated prostaglandin F<sub>2α</sub> (PGF<sub>2α</sub>) production in cultured bovine luteal cells. Inhibitors of RNA and protein synthesis (actinomycin D and cycloheximide, respectively) completely blocked TNF-α-stimulated PGF<sub>2α</sub> production. The phospholipase A<sub>2</sub> inhibitor, aristolochic acid, prevented TNF-α-stimulated, but not basal, PGF<sub>2α</sub> production, whereas the phospholipase C inhibitor, compound <span><math><mtext>48</mtext><mtext>80</mtext></math></span>, was without effect. The addition of arachidonic acid to cultures did not overcome the inhibitory effects of cycloheximide or aristolochic acid. In conclusion, TNF-α-stimulated prostaglandin production by bovine luteal cells is dependent upon the stimulation of phospholipase A<sub>2</sub> through mechanisms which require synthesis of RNA and protein.</p></div>","PeriodicalId":20653,"journal":{"name":"Prostaglandins","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0090-6980(96)00104-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19911957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 40
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