Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of B. pertussis vaccine on the serum glucose level of mice was investigated. The results show that at least two components in the vaccine interfere with glucose metabolism. A heat-stable component which is assumed to be LPS induced hypoglycemia 3-5.5 h after inoculation, especially in LPS-sensitized mice. A heat-labile component which is possibly equivalent with the LPF/HSF/IAP complex, is responsible for persistence of the hypoglycaemia for at least 6 days. If hypoglycaemia contributes to the neurological side effects after pertussis vaccination both components have to be considered as being responsible for these effects.
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PMID:A biphasic serum glucose response in mice to inoculation with pertussis vaccine. 673 46

Developmental changes in the responses of rat ventral prostate to isoproterenol (IPR) and forskolin (F) were studied in relation to the function of beta-adrenoceptor-adenylate cyclase system. The response of adenylate cyclase in the tissues to IPR at 10(-7)M and above was steadily enhanced after birth and reached a maximum at 12 weeks, followed by a decrease with age. In contrast, the response of the enzyme to F at 10(-7)M and above was highest at 2 weeks, but thereafter decreased. The changes in the response of the enzyme to IPR coincided with changes in the beta-adrenoceptor density and the binding ability of GTP binding proteins (G proteins) to GTP. The ADP-ribosylation of inhibitory G proteins (Gi proteins) catalyzed by pertussis toxin (IAP) decreased 70% in the tissues from 4 to 8 weeks, and then maintained this level. On the other hand, the ADP-ribosylation of stimulatory G proteins (Gs proteins) catalyzed by cholera toxin (CT) increased only 20% in the tissues from 2 to 4 weeks. Thus, the ratio of ADP-ribosylation of Gs to that of Gi significantly increased from 4 weeks, reaching a maximum at 12 weeks, but thereafter decreased gradually with age. These changes paralleled those in the function of G proteins and the response of the enzyme to IPR. It is suggested that the rapid and marked decrease in apparent level of Gi proteins in the rat ventral prostate after 4 weeks may have a key role in controlling the function of the beta-adrenoceptor-adenylate cyclase system in the tissues.
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PMID:Age-dependent changes in response of rat prostatic tissues to isoproterenol and forskolin: changes with sexual maturation in function of G proteins. 747 48

The N-acetyl glucosamine (GlcNAc)-specific lectin Datura stramonium agglutinin (DSA) rapidly and sugar-specifically released histamine from rat peritoneal mast cells, and pertussis toxin (IAP) inhibited it, suggesting that DSA activated mast cells via an IAP-sensitive G protein pathway. The additive effects of DSA and basic secretagogues such as compound 48/80 that activate IAP-sensitive G protein directly suggest that they shared the same mechanism of action including involvement of the IAP-sensitive G protein. Using lectin-blotting, blots of the corresponding glycoproteins detected by DSA diminished by haptenic sugar or pretreatment of the cells with N-glycosidase F, suggesting that the binding of DSA was responsible for the mast cell activation. The other GlcNAc-specific lectins such as Phytolacca americana mitogen, Solanum tuberosum agglutinin and wheat germ agglutinin (WGA) inhibited the histamine release induced by DSA, suggesting that these lectins were antagonists, but DSA was an agonist. Sialic acid-specific Macckia amurensis mitogen (MAM) inhibited the histamine release, and neuraminidase-treatment decreased mast cell activation induced by DSA. At least four mast cell glycoproteins that have affinity to DSA, WGA and MAM and are sensitive to neuraminidase-treatment were detected by lectin-blotting. Some of them may be binding sites coupled to histamine release including the IAP-sensitive G protein pathway. DSA is a useful tool for studying signal transduction of mast cells including the involvement of the IAP-sensitive G protein.
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PMID:Datura stramonium agglutinin released histamine from rat peritoneal mast cells that was inhibited by pertussis toxin, haptenic sugar and N-acetylglucosamine-specific lectins: involvement of glycoproteins with N-acetylglucosamine residues. 753 33

Using front-surface fluorometry and fura-2, the effect of endothelin (ET) on the cytosolic Ca concentration, (Ca)i, in smooth muscle cells and endothelial cells was determined. Both the contraction of smooth muscle cells and the release of endothelium-derived relaxing factor (EDRF) from endothelial cells are regulated by changes in (Ca)i. During contractions induced by U-46619, a thromboxane A2 analog, low doses of ET-1 induced an EDRF-dependent reduction of (Ca)i and force in porcine coronary arterial smooth muscles. Using porcine aortic valvular strips, we recorded the signals of (Ca)i in endothelial cells in situ. ET-1 induced an influx of Ca, which was markedly inhibited by pertussis toxin (IAP), thus indicating that this influx was regulated by an IAP-sensitive G-protein. BQ-123, a selective ETA receptor antagonist, partially inhibited the elevation of (Ca)i induced by ET-1, but did not affect the elevation of (Ca)i induced by ET-3. The sequence of cDNA encoding the porcine ETA receptor has been previously determined, and RT-PCR confirmed that ETA receptor mRNA was present in the endothelial cells on the aortic side of the valvular strips. Therefore, in addition to ETB receptors, functioning ETA receptors and ETA receptor mRNA can also be found in endothelial cells in situ. Thus, ET-1 may play an important role in controlling the coronary artery tonus not only by acting directly on smooth muscle cells to increase the force in a paracrine manner, but also by acting on endothelial cells to release EDRF in an autocrine manner, resulting in relaxation of smooth muscle cells.
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PMID:The effects of endothelin on vascular tonus. 758 Oct 32

A comparative study of hGH and IL2 post-signaling effects, as examined by RNA expression (Nb29) and protein levels of the heat-shock protein hsp70, was performed in a hormone-dependent rat lymphoma cell line, Nb2-11C. Optimal doses of hGH or IL2 increased Nb29 expression in a dose-dependent manner. Addition of both mitogens to cell cultures affected Nb29 expression and mitogenesis synergystically, indicating a possible interaction between the post-receptoral mechanisms of these mitogens. Pretreatment of the cells with cholera toxin (CT) inhibited Nb29 expression, protein levels and mitogenesis of hGH- or IL2-induced cells up to 50%, indicating the involvement of Gs-proteins in the post-signaling processes of both hGH and IL2. Incubation of cell cultures with low concentrations of pertussis toxin (IAP) (0.01 ng/ml) markedly increased Nb29 expression in hGH but not in IL2-induced cells, suggesting specific involvement of the Gi-protein in post-signaling processes of hGH-induced cells. Addition of the PKC activator 12-O-tetra-decanoyl phorbol ester (TPA) to control cell cultures markedly increased the expression of Nb29 RNA levels but not mitogenesis, indicating that induction of these proteins in the cells is not sufficient for cell proliferation. Furthermore, incubation of hGH- or IL2-induced cells with the potent PKC inhibitor staurosporin (ST) decreased the levels of Nb29 in both hGH- and IL2-induced cells, although the effect of the mitogens differed significantly in their inhibition slopes. These results indicate that activation of PKC is one of the signaling pathways differentially involved in hGH and IL2 stimulation of cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of heat-shock protein (hsp70) gene expression by hGH and IL2 in rat Nb2 lymphoma cells. 785 20

1. The metabotropic glutamate (mGlu) response was investigated in dissociated rat hippocampal CA1 pyramidal neurones using conventional and nystatin-perforated whole-cell modes of the patch recording configuration. 2. In the perforated patch recording configuration, the application of glutamate (Glu), quisqualate (QA), aspartate (Asp) and N-methyl-D-aspartate (NMDA) induced a slow outward current superimposed on a fast ionotropic inward current, whereas alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and kainate (KA) induced only an ionotropic inward current at a holding potential (VH) of -20 mV. A specific agonist of the mGlu receptor (mGluR), trans-1-aminocyclopentane-1,3-dicarboxylate (tACPD), induced an outward current in approximately 80% of the neurones tested. Asp- and NMDA-induced outward currents were antagonized by D-2-amino-5-phosphonopentanoate (D-AP5) whereas Glu-, QA- and tACPD-induced outward currents were not antagonized by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D-AP5, indicating that the mGlu response is an outward current component. 3. L-2-Amino-3-phosphonopropionate (L-AP3) and DL-2-amino-4-phosphonobutyrate (AP4) did not block the mGlu response. 4. The relative potencies of mGlu agonists were QA > Glu > tACPD. The threshold and EC50 values of metabotropic outward currents were 10-100 times lower than those of the ionotropic inward current (iGlu response). 5. The reversal potential of the mGlu response (EmGlu) was close to EK (K+ equilibrium potential), and it shifted 59.5 mV for a tenfold change in extracellular K+ concentration. 6. In Ca(2+)-free external solution, the mGlu response was elicited by an initial application of Glu, but subsequent applications failed to induce the response. There was also an increase in the intracellular free Ca2+ concentration ([Ca2+]i) during the application of Glu and QA but not of AMPA, indicating Ca2+ release from an intracellular Ca2+ store. 7. During the activation of a Ca(2+)-dependent K+ current (IK(Ca)) by inositol trisphosphate (IP3) in the internal solution, the mGlu response was suppressed. Addition of GDP-beta-S, neomycin or heparin to the internal solution also suppressed the mGlu response, but staurosporine had no effect. The mGlu response was abolished by pretreatment with either caffeine or ryanodine, but treatment with pertussis toxin (IAP) for 6-8 h had no effect. 8. The mGlu response was suppressed by tetraethylammonium, but not by either apamin or iberiotoxin, suggesting that intermediate-conductance Ca(2+)-dependent K+ (KCa+) channels are involved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat. 791 30

Pertussis toxin (islet-activating protein, IAP) sensitive guanine nucleotide-binding regulatory (G) proteins were quantitatively determined using [32P]ADP-ribosylating response in the platelet membranes prepared from patients with affective disorders (3 bipolar, 10 major depression) and sex- and age-matched controls. IAP-catalyzed [32P]ADP-ribosylation was not significantly different between patients and controls, suggesting that the quantity of IAP-sensitive G proteins is unaltered in affective disorder patients. The implication of this result was discussed with special reference to the previous reports dealing with the role of G proteins in affective disorders.
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PMID:Platelet pertussis toxin-sensitive G proteins in affective disorders. 796 69

To examine the biological role of adenosine A1 receptors in bovine pulmonary artery endothelial cells, we measured intracellular Cl-concentration [Cl-]i, using 10mM 6-methoxy-N-(3-sulfopropyl) quinolinium monohydrate (SPQ). N6-cyclopentyladenosine (CPA), a selective A1 agonist, at 10(-8)M to 10(-5)M, rapidly decreased [Cl-]i by 30% to 51%, without a rapid elevation in [Ca2+]i and cyclic AMP. This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin (IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker). We conclude that an A1 receptor in endothelial cells activates Cl- efflux via a PTX-sensitive G protein.
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PMID:Adenosine induces C1- efflux in endothelial cells via a pertussis toxin-sensitive G protein. 798 May 89

Insulin/dexamethasone/methylisobutylxanthine (hormones/IBMX) induce 3T3-L1 fibroblasts to differentiate into adipocytes. Our previous study suggested that pertussis toxin (IAP)-sensitive GTP-binding protein(s) (G-protein) is involved in the process of differentiation by hormones/IBMX, accompanied by c-fos induction. Northern blotting indicated that among the IAP-sensitive G-proteins, the levels of Gi2 alpha, Go alpha, and Gi3 alpha mRNA were decreased, increased and unchanged, respectively. Gi1 alpha was undetectable and IAP attenuated the decrease in Gi2 alpha mRNA level but did not affect the change in Go alpha mRNA level during the adipocyte differentiation. These results indicate that IAP-sensitive Gi2 alpha mRNA level is decreased during adipocyte differentiation. A combination of phosphatidylinositol-specific phospholipase C (PI-PLC) and IBMX induced c-fos expression in 3T3-L1 fibroblasts similar to that induced with hormones/IBMX. c-fos induced by both stimulators was also diminished by anti-inositolglycan antibody or anti-PI-PLC antiserum. Insulin stimulated the release of inositolproteoglycan and diacylglycerol from 3T3-L1 fibroblasts, which was suppressed by IAP treatment. These findings suggested that one of the pathways of adipocyte differentiation induced by hormones/IBMX occurs via the inositolglycan-specific PI-PLC cascade coupled to IAP-sensitive G-protein(s). Both activation of glycerophosphate dehydrogenase and stimulation of insulin-dependent 2-deoxyglucose uptake induced by hormones/IBMX were enhanced in protein kinase C-depleted cells exposed to phorbol 12-myristate 13-acetate (PMA), and attenuated in IAP-treated cells. The level of a 32P-labeled 52 kDa protein in plasma membrane fractions immunoprecipitated by anti-PI-PLC antiserum was increased by PMA stimulation, abolished in PMA-treated cells, and increased in IAP-treated cells. These findings suggest that protein kinase C phosphorylates PI-PLC, resulting in a decrease in PI-PLC activity related to the signal transduction pathway of adipocyte differentiation of 3T3-L1 fibroblasts.
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PMID:Possible involvement of phosphatidylinositol-specific phospholipase C related to pertussis toxin-sensitive GTP-binding proteins during adipocyte differentiation of 3T3-L1 fibroblasts: negative regulation of protein kinase C. 798 Dec 46

1. We designed a new method to determine quantitatively the intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ, using front-surface fluorometry and fura-2-loaded porcine aortic valvular strips. Using this method, we investigated the characteristics of the G-protein involved in endothelin-1 (ET-1)-induced changes in [Ca2+]i of endothelial cells in situ. 2. Endothelial cells were identified by specific uptake of acetylated-low density lipoprotein labelled with 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate (DiI-Ac-LDL). Double staining with DiI-Ac-LDL and fura-2 showed that the valvular strip was covered with a monolayer of endothelial cells and that the cellular component which contributed to the fura-2 fluorescence, [Ca2+]i signal, was exclusively endothelial cells. 3. ET-1 (10(-7) M) induced an elevation of [Ca2+]i consisting of two components: the first was a rapid and transient elevation to reach a peak, followed by a second, sustained elevation (the second phase). The first phase was composed of extracellular Ca(2+)-independent and -dependent components, while the second phase was exclusively extracellular Ca(2+)-dependent. The extracellular Ca(2+)-independent component of the first phase was due to the release of Ca2+ from intracellular storage sites. The second phase and part of the first phase of [Ca2+]i elevation were attributed to the influx of extracellular Ca2+. The Ca2+ influx component was completely inhibited by 10(-3) M Ni2+ but was not affected by 10(-5) M diltiazem. 4. Pertussis toxin (IAP) markedly inhibited the extracellular Ca2+-dependent elevation of [Ca2+]j, but had no effect on the extracellular Ca2+-independent elevation of [Ca2+], caused by ET-1 (10-7M).5. Bradykinin (10-7 M) or ATP (10- 5M) elevated [Ca2+]i and these responses also consisted of extracellular Ca2+-independent and extracellular Ca2+-dependent components. IAP had no effect on either component of the [Ca2+]i elevation induced by bradykinin or ATP.6. From these findings we conclude that, in porcine endotheliel cells in situ, ET-1 elevates [Ca2+]i as are result of a Ca2+ influx component from the extracellular space and release of intracelluarly stored Ca2+ .The Ca2+ influx is regulated by an IAP-sensitive G-protein, while the release of Ca2+ from the intracellular store is not.
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PMID:Sensitivity of G-protein involved in endothelin-1-induced Ca2+ influx to pertussis toxin in porcine endothelial cells in situ. 803 27


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