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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported that BSF-1 and an alloantibody to the B-cell differentiation antigen Lyb2 induce class II gene expression in two Ia negative pre-B-cell lines. Two questions were asked in these studies. The first question is whether the different stimuli which we and others have shown to induce class II expression in B-cells act via the same signal transduction mechanisms. The second question is whether the traditionally accepted pathway of B-cell differentiation, as defined by immunoglobulin (Ig) gene rearrangement, is applicable to other events that occur during B-cell differentiation. In this report, we have therefore examined a large panel of pre-B-cell lines at different stages of Ig gene rearrangement in an attempt to 1) identify the stage in B-cell development where class II gene expression occurs and where it becomes inducible by BSF-1 or anti-Lyb2, and 2) compare the signal transduction mechanisms used by these ligands. The majority of pre-B-cell lines tested did not express BSF-1 receptors and were consequently noninducible for class II by BSF-1; such cell lines were, however, inducible for class II expression by anti-Lyb2 and, in addition, by antibodies to the B220 membrane glycoprotein. The induction of class II molecules by BSF-1 and by anti-Lyb2 and anti-B220 differed in several respects: 1) Induction by anti-Lyb2 and anti-B220 did not require the presence of BSF-1 receptors; 2) BSF-1 selectively induced class II antigen expression while anti-Lyb2 and anti-B220 induced the expression of other surface markers as well; and 3) PGE2 inhibited BSF-1 but not antibody-mediated class II induction. Finally, the presence of receptors for BSF-1 and the baseline expression of cell surface Ia was shown to be unlinked to Ig gene rearrangement and expression in this series of pre-B-cell lines. The independent regulation of Ia and Ig genes observed here may reflect a branching rather than a linear pathway for B-cell differentiation. The differentiation of pre-B-cells to mature Ig-secreting cells should probably not be defined solely by rearrangement of Ig genes, since this is likely to represent an oversimplified view of B-cell differentiation.
J Mol Cell Immunol 1988
PMID:Differential induction of class II gene expression in murine pre-B-cell lines by B-cell stimulatory factor-1 and by antibodies to B-cell surface antigens. 315 Oct 65

Prostaglandin-H-synthase (PHS) peroxidase has been suggested to mediate drug metabolism particularly in extrahepatic tissues low in monooxygenase (MFO) activity. PHS can oxidize various xenobiotics in vitro; its contribution in vivo is still uncertain and is currently assessed by differences in the MFO- and PHS-catalyzed product/adduct formation of a few suitable substrates. Cells in culture that are PHS competent but MFO deficient can provide an additional approach for further investigating the role of PHS in the metabolic activation of foreign compounds. To this end, a cell line has been derived from ram seminal vesicles (SEMV), a tissue known as a good source of PHS but shown to be devoid of MFO activity. SEMV cells can be cultured in IBR or in RPMI medium supplemented with fetal calf serum, and have been subcultured until passage 30. The arachidonic acid (AA) metabolism in these cells has been characterized: besides incorporation in the lipid pool, AA was mainly metabolized to prostaglandin (PG) E2; minor products were PGF2 alpha and the lipoxygenase products 12- and 15-HETE. The PGE2 production (17 nmol/10(6) cells.24 h) of SEMV cells (passage 10) exceeded at least 10-fold that of other cells cultured under similar conditions. These data, indicative of high PHS activity, suggest that the cells can be a useful tool for future studies on the objectives outlined above.
Mol Toxicol
PMID:Prostaglandin-H-synthase competent cells derived from ram seminal vesicles: a tool for studying cooxidation of xenobiotics. 315 3

ProLHRH contains the luteinizing hormone-releasing hormone (LHRH) decapeptide and a 56 amino acid peptide designated gonadotropin-releasing hormone-associated peptide (GAP). We studied the effects of various known secretagogues of LHRH on the in vitro release of proLHRH fragments from the median eminence (ME) and subsequently characterized these immunoreactive products according to molecular weight (MW). GAP- and LHRH-like immunoreactive (LI) materials were secreted simultaneously into the media under basal conditions. Prostaglandin E2 stimulated release of both peptides by approximately 2-fold. Both phorbol ester and [K+] stimulated release of GAP-LI by 4-fold and LHRH-LI by 9-fold over baseline levels. When materials from [K+]-stimulated media were separated according to MW by high performance size-exclusion chromatography, a single peak eluted at 1300 MW in the same position as synthetic LHRH. Two GAP-LI peaks were observed. One eluted in the void volume, while the predominant peak co-eluted with synthetic rat GAP1-56 at approximately 6500 MW. These results indicate that GAP and LHRH are co-secreted, that they are released as intact peptides, and that activation of different intracellular pathways may cause their differential secretion. These results emphasize the importance of using both in vitro and chromatographic methodologies to evaluate the changes which may occur in LHRH prohormone processing and secretion.
Mol Cell Endocrinol 1988 Jan
PMID:Differential secretion of proLHRH fragments in response to [K+], prostaglandin E2 and C kinase activation. 328 35

Copper (Cu) and PGE2 are known to stimulate LHRH release from explants of the median eminence area (MEA) by two mechanisms distinguishable by their Ca2+ dependence. Moreover, exposure to Cu and PGE2 results in an amplified release of LHRH which is partially Ca2+ dependent, thus, resembling the release process stimulated by PGE2 alone. We have shown that LHRH release stimulated by Cu alone is Na+/Cl- dependent. By defining the Na+/Cl- dependence of PGE2- and Cu/PGE2-stimulated release of LHRH, we wished to ascertain if there is synergism between Cu and PGE2 actions. MEA of adult male rats were incubated for 5 min with 150 microM Cu and then for 15 min with 10 microM PGE2 (Cu/PGE2). Controls were incubated with Cu or PGE2. LHRH release into the medium was evaluated by RIA. Substituting Cl- in the incubation buffer with the non-permeant anion, isethionate, did not alter PGE2 stimulation of LHRH release, but it drastically inhibited Cu/PGE2 stimulation of LHRH release, indicating that this process requires a permeant monovalent anion. PGE2 and Cu/PGE2 stimulation of LHRH release were both inhibited when Na+ was substituted with Li+, or when 0.5 mM ouabain was included in the Na+-containing buffer; neither 10 microM tetrodotoxin (TTX) nor 100 microM amiloride were inhibitory. To ascertain if Na+ is required for Cu uptake, we evaluated the uptake of 67Cu by MEA explants and found that neither ouabain nor Li+ inhibited uptake, indicating that the extracellular Na+ and the activity of Na+/K+ ATPase are required for the process of LHRH release.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Endocrinol 1988 Mar
PMID:Evidence for synergism between copper and prostaglandin E2 in stimulating the release of gonadotropin-releasing hormone from median eminence explants: Na+/Cl- requirements. 328 21

Cardiac muscle cell injury may be related to metabolic changes associated with a rise in intracellular calcium. The mechanisms by which an elevated Ca2+ can cause injury are uncertain, but injury could occur by activation of any one or several calcium-dependent processes. To examine whether the process is mediated by prostaglandins (PG) or leukotriens (LT), we measured the successive release of creatine kinase (CK), PGE2 and LTC4 that have been reported to induce the cell injury via the arachidonic acid cascade, to the culture medium from myocardial cells under hypoxic or aerobic conditions. CK release, a biochemical marker of muscle cell necrosis, was first detected in the medium of hypoxic cultures at 9 h. Both PGE2 and LTC4 production and release were delayed, being first detected at 12 h after initiating hypoxia treatment. Addition of exogenous PGE2 or LTC4 to the culture medium (1.0 or 10 ng/ml) did not cause any effect on the CK release under aerobic condition. Cyclooxygenase inhibitor, indomethacin (1 X 10(-5) M) or lipoxygenase inhibitor, AA861 (1 X 10(-5) M), reduced the synthesis of PGE2 by 80% or LTC4 by 68% under hypoxia, respectively, but caused no beneficial effect on the CK release. These findings suggest that cardiac muscle cells themselves produce PGE2 and LTC4 after hypoxia and that the production of these compounds merely occurs as a result, but not as a cause of cell injury.
J Mol Cell Cardiol 1987 Jun
PMID:Stimulated synthesis of prostaglandin E2 or leukotrien C4 from myocardial cells is not a cause but a result of their injury under hypoxia. 347 55

In spontaneously atherosclerosis-susceptible White Carneau pigeons intimal cushions are noted consistently at the coeliac branch of aorta at birth. While these cushions do not progress into atherosclerotic lesions, the area across from the cushion (so called "lesion area") develop a classic atherosclerotic plaque by three years of age. In order to explain this regional aortic susceptibility to atherosclerosis, cholesterol and cholesteryl ester concentrations and prostaglandin biosynthesis in the two aortic regions were examined. It was found that the concentration of free and esterified cholesterol was higher in the intimal cushion area. Examination of the formation of various prostaglandins from C14-arachidonic acid indicates a striking increase in PGE2 synthesis in the lesion area with no difference in the formation of 6-keto PGF1 alpha (stable product of PGI2). These studies suggest that one of the earliest changes noted in the "lesion area" that differs from the intimal cushion is the enhanced formation of PGE2.
Virchows Arch B Cell Pathol Incl Mol Pathol 1981
PMID:Regional aortic differences in atherosclerosis susceptibility. Relationship to lipid concentration and prostaglandin biosynthesis. 611 22

In spontaneously atherosclerosis-susceptible White Carneau pigeons, intimal cushions that appear at birth near the coeliac branch of aorta do not progress into atherosclerotic lesions. However, the area across from the intimal cushion (so called 'lesion area') a) accumulates cholesteryl esters b) synthesizes more PGE2 and c) eventually develops into complicated atherosclerotic plaques. When DOCA-salt hypertension is induced in the pigeons, the 'initimal cushion' area displays a) accumulation of increasing amounts of cholesteryl esters and b) increase in the synthesis of all prostaglandins (particularly PGE2) from C14-arachidonic acid and c) approaches similarity to the 'lesion area' in the magnitude of these changes. These results suggest that under the influence of a risk factor, the 'intimal cushion' can acquire biochemical properties of the atherogenic areas of the aorta.
Virchows Arch B Cell Pathol Incl Mol Pathol 1981
PMID:Regional aortic differences in atherosclerosis-susceptibility: changes in prostaglandin biosynthesis and cholesterol accumulation in response to desoxycorticosterone (DOCA)-salt induced hypertension. 611 75

[3H]PGE2 specifically bound to isolated glomeruli. The KD value and the number of sites were 80 nM and 528 fmoles/mg respectively. PGE1 and PGE2 resulted in equipotent inhibition of binding whereas PGI2 was markedly less active. It was not possible to demonstrate specific receptors for PGE2 in glomerular mesangial and epithelial cultured cells. PGE1, PGE2 and PGI2 (0.1-100 microM) stimulated cyclic AMP concentration both in isolated glomeruli and glomerular cultured cells. Basal cyclic AMP in epithelial cells was greater than in mesangial cells or glomeruli. The cyclic AMP accumulation in the presence of PGs was greatest in mesangial cells. Maximum stimulation was in the range 300-1400%. For the three preparations, PGE2 and PGE1 produced a greater effect than PGI2. ED50 values were identical for PGE1 and PGE2 (5 microM for epithelial cells and glomeruli, 20 microM for mesangial cells). ED50 value for PGI2 were lower than those for PGE1 or PGE2 (0.2, 2 and 5 microM for glomeruli, epithelial cells and mesangial cells, respectively). The effects of the three PGs were not additive when tested at maximally effective concentrations. These results demonstrate that PGE1, PGE2 and PGI2 stimulate glomerular and cellular cyclic AMP. A relationship between [3H]PGE2 binding sites and this biological effect has not been established. The physiological events secondary to the increase in glomerular cyclic AMP are also yet to be determined.
Mol Cell Endocrinol 1983 May
PMID:PGE2 binding sites and PG-stimulated cyclic AMP accumulation in rat isolated glomeruli and glomerular cultured cells. 613 4

Synthetic human pancreatic growth hormone-releasing factor (hpGRF(1-40)-NH2) causes a 100% stimulation of cyclic AMP cell content in rat adenohypophysial cells in culture as early as 1 min after its addition while a maximal 33-fold increase is measured at 40 min. Somatostatin (10 nM) causes a 40-60% inhibition of GRF-induced cyclic AMP accumulation while GH release is inhibited by 90-95% at all time intervals. The inhibitory effect of somatostatin is exerted on the maximal effect of GRF while the ED50 values of GRF action on cyclic AMP cell content (approximately 1 nM) and GH release (approximately 0.1 nM) are not affected by the tetradecapeptide. Prostaglandin E2 causes a 2.5-fold increase in cyclic AMP levels within 1 min after its addition with a maximal 25-fold stimulation measured at 30 min. Although not completely additive, the stimulatory effects of PGE2 and GRF together on cyclic AMP cell content and GH release are more potent than when either substance is present alone. The inhibitory effects of somatostatin on PGE2 action are analogous to those observed in the presence of GRF. The present data suggest that the hypothalamic control of GH secretion by GRF and somatostatin results, at least to a large extent, from the balance between the stimulatory action of GRF and the inhibition of somatostatin on the adenylate cyclase system.
Mol Cell Endocrinol 1983 Dec
PMID:Interactions between growth hormone-releasing factor, prostaglandin E2 and somatostatin on cyclic AMP accumulation in rat adenohypophysial cells in culture. 614 Jan 96

Our studies have shown that stimulation of human natural killer (NK) cells by poly I:C does not depend on or require monocytes. In contrast, the presence of monocytes in a mixed population of mononuclear cells stimulated by poly I:C suppresses NK activity. The suppression can be partially overcome if indomethacin (10(-6) M) is added to the culture during stimulation. Culture supernatants from poly I:C stimulated monocytes do not have detectable levels of anti-viral activity but contained appreciable amounts of PGE2. Our results offer an explanation as to how NK cells may protect themselves from suppression by PGE2. We have demonstrated that IFN-activated NK cells become resistant to PGE2-mediated suppression; moreover the suppression does not require cells other than the large granular lymphocytes, the major effector cell type for NK. Taken together, the data suggest that stimulation of NK cells is dependent on and regulated by the relative levels of interferon produced by lymphocytes and PGE2 produced by monocytes.
Mol Immunol 1982 Oct
PMID:Modulation of human NK cells by interferon and prostaglandin E2. 618 17


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