Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cultured rat aorta-derived A-10 cells, epidermal growth factor-urogastrone (EGF-URO) acts synergistically with arginine vasopressin (AVP) to augment the AVP-mediated release of 3H-arachidonate (3H-AA) from 3H-AA prelabeled cells. On its own, EGF-URO had no effect on AA release and had no effect on calcium influx or efflux either in the absence or presence of AVP. The synergistic action of EGF-URO was not affected by actinomycin D, cycloheximide, indomethacin, by the diacylglycerol lipase inhibitor U-57,908, or by the tyrosine kinase inhibitors genistein (GS) and tyrphostin (TP). TP did, nonetheless, completely abrogate 3H-thymidine incorporation triggered in the presence of EGF-URO. Although EGF-URO stimulated an increase in calpactin-II (lipocortin-I) phosphorylation in permeabilized cells, no such increase was detected in intact cells exposed to EGF-URO either alone or in combination with AVP, under conditions where EGF-URO augmented the action of AVP. The phospholipase A2 inhibitor, mepacrine, had no effect on AVP-mediated AA release, but abolished the synergistic action of EGF-URO. We conclude that in contrast with our previous results with gastric smooth muscle strips, wherein EGF-URO acts via the diacylglycerol lipase-mediated metabolism of diacylglycerol, and in keeping with observations with cultured mesangial cells, EGF-URO acts synergistically with AVP in A-10 cells via the activation of phospholipase A2. This synergistic action of EGF-URO does not appear to be due to increased levels of cyclooxygenase and would appear not to require increased tyrosine kinase activity.
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PMID:Synergistic actions of epidermal growth factor-urogastrone and vasopressin in cultured aortic A-10 smooth muscle cells. 138 68

Stromal vascular cells were isolated from adipose tissue obtained from three different anatomical locations: epididymal (EPI), retroperitoneal (RP), and dorsal subcutaneous (SC), and allowed to differentiate in primary tissue culture. Cell number, protein concentration, glycerophosphate dehydrogenase, and lipoprotein lipase activity were similar in cells obtained from the EPI, RP, and SC regions, as were total insulin binding and the affinity of insulin for its receptor. However, both maximal insulin receptor tyrosine kinase activity and insulin-stimulated phosphorylation of the insulin receptor were significantly lower (P less than 0.05) in cells cultured from the SC region. In addition, newly differentiated adipocytes from the SC region were less sensitive to the ability of insulin to stimulate glucose uptake, and maximal insulin-stimulated glucose uptake by these cells was also significantly lower (P less than 0.05) when compared to cells obtained from the two other regions. Since these studies were performed on adipocyte precursor cells, allowed to differentiate to a similar degree in primary culture, the observed differences in insulin receptor phosphorylating activity, as well as the ability of insulin to stimulate glucose uptake appear to be intrinsic to adipose tissue from the three sites.
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PMID:Differences in insulin action as a function of original anatomical site of newly differentiated adipocytes obtained in primary culture. 165 46

Phospholipase (PL) A2 activity prepared from isolated rat fat pads incubated with sodium orthovanadate (vanadate) was increased in a time- and dose-dependent manner. The increasing effect of vanadate was reduced in the presence of tyrosine kinase inhibitors. Under the inhibition of protein synthesis by cycloheximide, vanadate still showed a full effect on the increase in PL A2 activity. Various PL A2 inhibitors, such as manoalide, quinacrine and p-bromophenacyl bromide, suppressed the stimulatory release of lipoprotein lipase (LPL) activity from the fat pads by vanadate. Moreover, the vanadate-stimulated release of LPL activity was decreased by the cyclooxygenase and thromboxane synthetase inhibitors, and a thromboxane A2 receptor antagonist, but was never suppressed by a lipooxygenase inhibitor. The stimulatory release of LPL activity by vanadate was also decreased in the presence of tyrosine kinase inhibitors. These results suggest that vanadate increases PL A2 activity, and the increase in PL A2 activity is partly involved in the vanadate-stimulated release of LPL activity with an association to the membrane tyrosine kinase.
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PMID:Sodium orthovanadate increases phospholipase A2 activity in isolated rat fat pads: a role of phospholipase A2 in the vanadate-stimulated release of lipoprotein lipase activity. 774 10

Cerebellar neurons, cultured on monolayers of 3T3 fibroblasts or on a polylysine/laminin-coated substratum, responded to recombinant basic FGF by extending longer neurites. The response was biphasic reaching a maximum at 5 ng/ml FGF, but desensitising at 100-200 ng/ml FGF. The response to FGF could be inhibited by a tyrosine kinase inhibitor (the erbstatin analogue), by a diacylglycerol lipase inhibitor (RHC-80267) and by a combination of N- and L-type calcium channel antagonists or other agents that negate the effects of calcium influx into neurons. The response to FGF could be fully mimicked by arachidonic acid added directly to the cultures, or generated via activation of phospholipase A2 with melittin. The response to melittin, but not to FGF or arachidonic acid, was inhibited by 4-bromophenacyl bromide, a phospholipase A2 inhibitor. The response to arachidonic acid was also biphasic and high concentrations of this agent could cross-desensitise the FGF response and vice versa. The response to arachidonic acid could be fully inhibited by the agents that block or negate the effects of calcium influx into neurons, but was not inhibited by the tyrosine kinase or diacylglycerol lipase inhibitors. These data suggest that FGF stimulates neurite outgrowth by activating a cascade that involves activation of phospholipase C gamma to produce diacylglycerol, conversion of diacylglycerol to arachidonic acid by diacylglycerol lipase and the activation of voltage-gated calcium channels by arachidonic acid.
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PMID:Characterisation of the second messenger pathway underlying neurite outgrowth stimulated by FGF. 805 Mar 74

In guinea pig gastric longitudinal (LM) and circular (CM) muscle strips, angiotensin-II (Ang-II) caused a concentration-dependent contraction that required extracellular calcium and that could not be attributed to the secondary release of agonists from neural elements. Contractions in both the LM and CM were blocked by the Ang-II AT1 receptor antagonist, Losartan (DuP 753, pA2 9.1) but not by the AT2 antagonist, PD 123319. However, in the LM preparation, indomethacin (3 microM) blocked Ang-II-mediated contraction, whereas in the CM contraction was resistant to indomethacin. Contractions caused by Ang-II in the CM preparations were also unaffected by inhibitors of leukotriene biosynthesis, but were partially (58%) inhibited by the cytochrome P450 monooxygenase inhibitor, ketoconazole. The diacylglycerol lipase inhibitor, U57,908, at a concentration (20 microM) that completely blocked the contractile action of epidermal growth factor in the LM, caused a substantial inhibition of Ang-II-mediated contraction in both the LM (55% inhibition) and CM (75% inhibition). The phospholipase A2 inhibitor, mepacrine caused a modest inhibition (24%) of contraction in both preparations. In the presence of U57,908, mepacrine further inhibited contraction caused by Ang-II in the LM preparation. The tyrosine kinase (YK) inhibitors, genistein and tyrphostin (RG 50864) selectively and completely blocked Ang-II-mediated contraction in the LM, without affecting contractions caused by carbachol and bradykinin. In the CM preparation, the two YK inhibitors were selective, but only partially (40-60%) blocked Ang-II-mediated contraction, without affecting contractions caused by bradykinin and carbachol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distinct signal transduction pathways for angiotensin-II in guinea pig gastric smooth muscle: differential blockade by indomethacin and tyrosine kinase inhibitors. 843 35

This study examined the differences in mechanisms of toxicity when adipose cells from males and females were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Glucose uptake by adipose tissue in vitro was decreased significantly in male guinea pigs within 1 d of intraperitoneal injection of TCDD, but there was no significant effect in females, even at 28 d after treatment. A similar difference between male and female guinea pigs was detected in the effect of TCDD on lipoprotein lipase (LPL) activity, except that a significant decrease in LPL activity was observed 28 d after treatment. Experiments with adipose tissue explants from untreated guinea pigs and macaques revealed similar gender differences in the effect of TCDD in vitro on glucose uptake and LPL activity. Both time-course studies and dose-response studies with TCDD in vitro confirmed the greater sensitivity of male tissues to TCDD toxicity. TCDD induced lipid peroxidation in the adipose tissues of male guinea pigs, while it had no effect in females. 3H-TCDD binding affinity studies in adipose explant tissues showed that tissues from male guinea pigs and monkeys had a higher binding capacity for TCDD than female tissues. TCDD induced a significant reduction in nuclear protein phosphorylation and an increase in cytosolic protein phosphorylation in adipose tissue from male guinea pigs; the effects in female tissues were opposite: nuclear protein phosphorylation increased and cytosolic protein phosphorylation decreased. In a cell-free system in the absence of the nucleus, adipose tissues from male guinea pigs and monkeys responded to TCDD with a rapid stimulation of tyrosine kinase activity but female tissues from both species had a significantly lower and slower response. TCDD induced the DNA binding of AP-1 in adipose tissues of male guinea pigs, but in female tissues TCDD reduced the DNA binding of AP-1. In summary, the results of this study demonstrate gender differences in the response of nonreproductive cells to TCDD. Some of these differences involve different mechanisms of toxicity in both the cytoplasmic and nuclear compartments of the cell.
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PMID:Gender differences in the mechanism of dioxin toxicity in rodents and in nonhuman primates. 888 12

Mechanisms of the stimulatory release of lipoprotein lipase (LPL) activity from isolated rat fat pads by sodium orthovanadate (vanadate) were studied through a cAMP-dependent process. A potent inhibitor of insulin receptor tyrosine kinase, quercetin, inhibited the vanadate-increasing effect on the LPL activity in fat pads, but did not inhibit the vanadate-stimulated release of LPL activity from the fat pads. Propranolol and N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) decreased the vanadate-stimulated release in a dose-dependent manner. Isoproterenol and dibutyryl cAMP (Bt2cAMP) stimulated the release of LPL activity from fat pads. Vanadate, as well as isoproterenol, rapidly increased the cAMP content in fat pads, and this increase was almost completely inhibited by propranolol. Vanadate increased the cAMP-dependent protein kinase (PKA) activity ratios calculated from the measurement in the presence or absence of cAMP or PKa inhibitor. These results suggest that the vanadate-stimulated release of LPL activity is associated with a process involving a rapid increase in the cAMP content accompanied by the activation of PKA.
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PMID:Involvement of the rapid increase in cAMP content in the vanadate-stimulated release of lipoprotein lipase activity from rat fat pads. 895 Nov 55

We have evaluated the signal transduction pathways whereby, in comparison with epidermal growth factor-urogastrone, ethanol causes a rapid contractile response in guinea pig gastric longitudinal muscle. As for epidermal growth factor (EGF), the ethanol-induced contraction required extracellular calcium, was sensitive to the tyrosine kinase inhibitors genistein and tyrphostin 47 (AG213), and was blocked by both the cyclo-oxygenase inhibitor, indomethacin, and the diacylglycerol lipase inhibitor, U57908. The 50% effective concentration (EC50) for the contractile action of ethanol (approximately 140 mM) was lower than that for propanol and methanol and was not affected by the aldehyde dehydrogenase inhibitor, 4-methyl pyrazole. The actions of ethanol were distinct from those of EGF in that EGF-induced contractions were sensitive to the kinase C inhibitor GF109203X, and the EGF receptor kinase inhibitor PD153035, whereas ethanol-induced contractions were refractory to these inhibitors. Further, EGF-induced contractions were attenuated by the voltage-sensitive calcium channel antagonist, nifedipine, whereas the ethanol-induced contractile response was resistant to nifedipine but blocked by the "receptor-operated" calcium channel antagonist SKF96365. We conclude that ethanol without metabolism via alcohol dehydrogenase causes a contractile response in gastric longitudinal muscle tissue via a tyrosine kinase inhibitor-sensitive signal pathway that is parallel in many respects but yet is distinct from that activated by EGF.
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PMID:Tyrosine kinase inhibitor-sensitive contractile action of ethanol in gastric smooth muscle: comparison with the action of epidermal growth factor. 901 Sep 19

This study was performed to evaluate the effect of human recombinant basic fibroblast growth factor on arachidonic acid release from rat pancreatic acini and to determine the cellular mechanism involved. From enzymatic assays, basic fibroblast growth factor did not significantly stimulate phospholipase A2 activity, whereas it significantly increased diacylglycerol lipase activity. Validity of phospholipase A2 or diacylglycerol lipase inhibitors was confirmed by their ability to inhibit phospholipase A2 or diacylglycerol lipase activities. Basic fibroblast growth factor increased intracellular accumulation and extracellular release of arachidonic acid from metabolically labelled acinar cells in a concentration- and time-dependent manner. This effect was maximal with 50 pM basic fibroblast growth factor and became significant after a 5-min incubation period. The protein tyrosine kinase inhibitor, 0.5 mM genistein, inhibited arachidonic acid release in basic fibroblast growth factor-stimulated acini, whereas 100 microM vanadate, a protein tyrosine phosphatase inhibitor, enhanced arachidonic acid release. Two phospholipase A2 inhibitors, mepacrine and aristolochic acid, failed to attenuate basic fibroblast growth factor-stimulated arachidonic acid release. A diacylglycerol lipase inhibitor RHC 80267 at 150 microM and 50 microM completely inhibited 50 pM basic fibroblast growth factor-induced intracellular accumulation and extracellular release of arachidonic acid, respectively. Furthermore, basic fibroblast growth factor stimulated arachidonic acid release was also inhibited by 10 microM U73122 and by 100 nM staurosporine, phospholipase C and protein kinase C respective inhibitors. Wortmannin, an inhibitor of basic fibroblast growth factor-stimulated phospholipase D, did not affect arachidonic acid release. 100 nM 4 beta-phorbol 12-myristate 13-acetate also increased arachidonic acid release, an effect also inhibited by staurosporine. Taken together, these data demonstrate activation of diacylglycerol lipase and arachidonic acid release in pancreatic acini upon stimulation by basic fibroblast growth factor, and strongly indicate that arachidonic acid release in response to basic fibroblast growth factor depends upon the sequential action of tyrosine kinase, phospholipase C, protein kinase C and diacylglycerol lipase but not from phospholipase A2 not phospholipase D activation.
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PMID:Basic fibroblast growth factor-stimulated arachidonic acid release in rat pancreatic acini: sequential action of tyrosine kinase, phospholipase C, protein kinase C and diacylglycerol lipase. 902 13

We observed a contractile action of ethanol (20-500 mM) and other alcohols (methanol and propanol, but not butanol) in guinea pig gastric longitudinal (LM) and circular (CM) smooth muscle preparations. The potency order for the alcohols in the LM preparation was: ethanol = propanol > methanol; and in the CM preparation, propanol > ethanol > methanol. Like epidermal growth factor-urogastrone (EGF), the contractile actions of ethanol in the LM and CM preparations required extracellular calcium and were blocked by the tyrosine kinase inhibitors, genistein and tyrphostin-47 (AG213). The tyrosine phosphatase inhibitor, pervanadate, potentiated the contractile action of ethanol in the LM preparation. Ethanol-induced contractions in both preparations were not affected by 4-methyl pyrazole, an inhibitor of alcohol dehydrogenase, and were unaffected by tetrodotoxin, atropine, prazosine or yohimbine. In the LM preparation, like EGF, the contractile action of ethanol was blocked by the cyclooxygenase inhibitor, indomethacin, and the diacylglycerol lipase inhibitor, U57,908; in the CM preparation, contractions caused by ethanol and EGF were still observed in the presence of these two inhibitors. Contractions caused by ethanol and EGF in the LM preparation were not affected by the epoxygenase inhibitor, ketoconazole; the lipoxygenase inhibitor, nordihydroguaiaretic acid; or the phospholipase A2 inhibitor, mepacrine. In contrast, in the LM preparation, EGF-induced contractions were attentuated by the EGF receptor-kinase inhibitor, PD153035; the MAP-kinase-kinase (MEK) inhibitor, PD98059; the kinase C inhibitor, GF109203X; and the phosphatidylinositol 3'-kinase inhibitors, Wortmannin and LY294002; whereas ethanol-induced contractions were unaffected by these inhibitors. Both ethanol and EGF caused small increases in the phosphotyrosyl protein content of the gastric tissue. We conclude that ethanol causes its contractile effects in the distinct gastric LM and CM preparations independent of nerve-released agonists and via a tyrosine kinase inhibitor-sensitive signal pathway that is in many respects similar to, but distinct from the one activated by EGF.
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PMID:Contractile action of ethanol in guinea pig gastric smooth muscle: inhibition by tyrosine kinase inhibitors and comparison with the contractile action of epidermal growth factor-urogastrone. 922 91


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