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T Zelles

Publications and source records attributed to T Zelles.

At least 55 records · Page 3Linked to original sources
PubMed1993

Cholecystokinin modulates isoproterenol induced changes in rat parotid gland.

1. Parotid gland secretory function and activity of several enzymes involved in intracellular second messenger signalling were measured in rats receiving 0.5 ml i.p. injections of saline (control), isoproterenol, CCK or both drugs. 2. Isoproterenol caused a 2.5-fold increase in parotid gland wet weight compared to control. Chronic administration of CCK alone has no effect on gland weight. A combination of CCK and isoproterenol did not alter the hypertrophy of the gland observed with isoproterenol alone. 3. Isoproterenol administration caused a 74% decrease in parotid gland amylase enzyme activity. While CCK alone did not influence the enzyme activity, it depressed amylase mRNA steady state levels and had an additive effect on further decreasing mRNA levels when administered in combination with beta-agonist. 4. Phospholipase C registered an increase ranging from 22 to 38% in all experimental groups as compared to control. 5. Parotid gland protein kinase C and PdtIns 3-kinase activity were not altered in response to CCK alone, but in combination with isoproterenol, appeared to moderate beta-agonist signal transduction responses.

Amylases↗
PubMed1992

Down-regulation of cellular proto-oncogenes during inhibition of rat parotid acinar cell proliferation.

The role of cell surface galactosyltransferase in mediating isoproterenol-induced parotid gland hypertrophy and hyperplasia was examined in rat parotid gland acinar cells. Introduction of the transferase modifier, alpha-lactalbumin, or galactosyltransferase-associated kinase inhibitor trifluoperazine, into beta-agonist-treated rats prevented acinar cell proliferation as determined by [3H]thymidine incorporation after 96 h of treatment. However, [3H]thymidine incorporation into DNA after 24 h of treatment, with injection of a combination of isoproterenol/alpha-lactalbumin or isoproterenol/trifluoperazine, was similar to injections of isoproterenol alone; suggesting that acinar cells could be stimulated to undergo a single round of DNA synthesis. Northern blot analysis of myc and fos expression followed a similar pattern of down-regulation to control levels after 96 h but not after 24 h. Hybridization with erb B showed little change with proliferation, confirming previous observations on protein levels of the EGF-receptor in acinar cells. Western blot analysis of nuclear protein expression of myc revealed that isoproterenol caused an increase in a 62-kDa protein which was again down-regulated with inhibition of cell proliferation. Analysis of protein levels of Rb110 protein showed no change in protein level in the nucleus with cell proliferation, but did show an associated increase in protein phosphorylation in response to growth stimulation.

Animals↗
PubMed1992

Cross reactivity among the ligands of the 7 helix family.

"Specific" drugs for receptors of the 7 helix family inhibited in high doses other receptors of the same family, as well. Atropine inhibited [3-H]-clonidine binding, beta-adrenergic drugs: propranolol, betoxalol, ICI 118.551 inhibited labelled QNB binding to all the 3 main subtypes of muscarinic receptors. Authors propose the existence of common features in the ligand binding sites of the receptors of 7 helix family.

Adrenergic beta-Antagonists↗
PubMed1991

Effect of nicotine on dopaminergic-cholinergic interaction in the striatum.

We have investigated the effect of nicotinic receptor stimulation on acetylcholine (ACh) release measured by radioassay in rat striatal slices. Since the release of ACh in the striatum is tonically inhibited by endogenous dopamine and nicotine enhances the release of dopamine, we studied the release of ACh when the dopaminergic input was impaired. We used chemical denervation (6-hydroxydopamine pretreatment) or D2-receptor-blockade by sulpiride to remove the dopaminergic control of the cholinergic neurons. In our experiments nicotine failed to increase ACh release from striatal slices taken from rats whose dopaminergic-cholinergic interaction was not impaired but it enhanced the release of ACh from slices dissected from 6-hydroxydopamine pretreated rats or in the presence of sulpiride. Our results provide neurochemical evidence for the existence of nicotinic receptors on striatal cholinergic interneurons. Since the spontaneous release of ACh enhanced by nicotine was inhibited by tetrodotoxin it seems very likely that (-)-nicotine acts on the somatodendritic part of cholinergic interneurons.

Acetylcholine↗
PubMed1991

Role of protein phosphorylation and inositol phospholipid turnover in rat parotid gland proliferation.

The involvement of protein phosphorylation in isoproterenol (ISO)-mediated proliferation in the rat parotid gland was investigated by labeling the cells with [32P] orthophosphate. An increased (4-6 fold) incorporation of the radiolabel was noted in the total parotid gland homogenates of ISO-treated animals when compared to controls. Plasma membrane, nuclear membrane and cytoplasm were isolated, the proteins separated by SDS/PAGE and the phosphoproteins detected by autoradiography. Two phosphoproteins with apparent Mr of 45 and 170 kDa were identified in the cytoplasm while the 170 kDa phosphoprotein also appeared as part of plasma membrane. Transfer of these proteins to nitrocellulose followed by Western blot detection with an antiphosphotyrosine monoclonal antibody showed reactivity with the 170 kDa region of the plasma membrane and cytoplasm. Separate in vitro studies involving incubations of rat parotid slices with 0.2 mM ISO and [3H] myo-inositol for 1 min induced inositol phosphate hydrolysis resulting in a significant increase in inositol-bis and -tris phosphate production. Inositol phosphate production can be blocked by pre-incubation with a mixed beta-adrenergic receptor antagonist but not with physiological concentrations of alpha- or beta 1-specific adrenergic receptor antagonists, indicating the ISO effects are mediated through the beta 2-adrenergic receptors. The inclusion of calmodulin antagonists along with ISO prevented the expression of cell-surface galactosyltransferase and retarded gland hypertrophy and hyperplasia. These results suggest that ISO treatment leads to the phosphorylation of target proteins which may be involved in signal transduction pathways leading to cell proliferation.

Animals↗
PubMed1990

Cell surface galactosyltransferase acts as a general modulator of rat acinar cell proliferation.

Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 galactosyltransferase. In this study, dietary changes causing acinar cell proliferation included the following: the introduction of animals to a liquid diet (causing gland atrophy) followed by reintroduction of solid chow, gustatory stimulation provided by the introduction of 0.5% citric acid to animal drinking water, and removal of the submandibular gland with subsequent reliance on the parotid gland for salivary protein. Alterations in growth factor levels were produced by injecting animals with a chronic (3 day) regimen of either nerve growth factor or epidermal growth factor. Parotid gland proliferation could be blocked in all cases except EGF by the injection of propranolol, a beta-adrenoceptor antagonist, or the galactosyltransferase specific modifier protein, alpha-lactalbumin. EGF-induced proliferation could, however, be prevented by treating the animals with monoclonal antibody to EGF receptor or galactosyltransferase modifier protein alpha-lactalbumin. These results for normal acinar cell proliferation suggest a direct role for cell surface beta 1-4 galactosyltransferase in signalling and maintaining active cell growth.

Animals↗
PubMed1990

Characterization of neuronal cholecystokinin receptor by L-364,718 in Auerbach's plexus.

The release of [3H]acetylcholine [( 3H]ACh) from Auerbach's plexus and the contraction of longitudinal muscle strips in response to the administration of cholecystokinin (CCK) were measured and recorded simultaneously. The peripheral CCK receptor antagonist, 3S(-)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepine-3-yl)-1H- indole-2-carboxamide (L-364,718), antagonized the ACh releasing effect of CCK in a dose-dependent manner. The IC50 value and the dissociation constant (KD) were 41.0 +/- 2.0 pM and 0.06 +/- 0.01 nM, respectively. These results suggest that L-364,718 is a very potent antagonist of the neuronal CCK receptors.

Acetylcholine↗
PubMed1990

Alpha adrenergic drugs inhibit [3H]-QNB binding to muscarinic receptors of rat heart, brain and parotid gland membranes.

Alpha adrenergic agonists and antagonists as clonidine, guanfacine, yohimbine, phenylephrine and prazosin inhibited the [3H]-QNB binding to rat brain cortex muscarinic acetylcholine receptor (mAChR, M-1 subtype), heart (M-2 subtype) and parotid gland homogenate (M-3 subtype) in a dose-dependent competitive fashion. Ki values were between 10(-6) and 10(-3) M. Hill coefficients were about 1. No correlation was found between mAChR inhibiting capacity of these drugs and their activity on alpha adrenergic receptors. In contrast, other transmitters, as dopamine, GABA, glutamic acid, histamine, serotonin, isoproterenol and platelet activating factor (PAF) did not affect the QNB binding.

Adrenergic alpha-Agonists↗
PubMed1990

Cell-surface galactosyltransferase acts as a modulator of rat and human acinar cell proliferation.

Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of beta 1-4 galactosyltransferase. In this study, dietary changes causing acinar cell proliferation included the following: the introduction of animals to a liquid diet (causing gland atrophy) followed by re-introduction of solid chow, gustatory stimulation provided by the introduction of 0.5% citric acid to animal drinking water, and removal of the submandibular gland with subsequent reliance on the parotid gland for saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, alpha-lactalbumin. Propranolol, a beta-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGF-induced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier alpha-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, muco-epidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier alpha-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface beta 1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.

Animals↗
PubMed1990

[Analysis of the effectiveness of pilocarpine in the management of xerostomia].

The authors have studied the "sympathetic like" side effect of pilocarpine after single injection (1 mg/100 g b.w., i.p.) of the drug. They developed a system for the continuous automatic recording the amylase activity of the saliva secreted by the parotid glands of rats, "in situ". Pilocarpine stimulus was characterized by a peak in amylase activity--regularly observed in the first 40-60 min--which was additive to the cholinergic amylase secretory response. After this the amylase secretion was continued with lower activity. The role of a beta-adrenergic component in the pilocarpine stimulus appears to be supported by the finding that propranolol (2.5 mg/100 g b.w., i.p.) pretreatment applied 30 min prior to the pilocarpine stimulus prevented the appearance of the characteristic amylase peak. These data support that the beta-adrenergic side effect triggering the periodical synthesis of export proteins during the course of pilocarpine treatment accounts for the selative efficiency of pilocarpine in the therapy of xerostomia.

Amylases↗
PubMed1990

[Production of antibodies for the detection of galactosyl transferase by immunologic methods].

Providing the export proteins with carbohydrate has an important role in operation of the saliva glans. For examining the UDP-Galactose: D-Glucose 4-Galactosyl-transferase (GT) functioning in the rat parotitis specific high purity policlonal antibodies have been prepared by means of repeated immunizig inoculation of rabbits. Thereby possibility of examination of the location and circulatory mechanism of the GT in parotitis acinus cells has been created.

Animals↗
PubMed1989

Effects of liquid diet on amylase activity and mRNA levels in rat parotid gland.

Rats maintained on this diet demonstrated a dramatic reduction in amylase enzyme activity. This reduced level was evident through quantitation based on activity per mg gland protein, as well as on activity per gland wet weight. This was confirmed by the densitometric scanning of Western blots of sodium dodecyl sulphate-polyacrylamide gels of total parotid gland protein. Immune precipitation of enzyme activity from cell lysates showed that liquid-diet animals had lower levels of amylase than chow-fed controls. Isolation of poly (A+)-containing RNA followed by in vitro translation indicated that the steady-state level of amylase-specific mRNA had increased relative to the total mRNA pool. This outcome was also observed by dot-blot analysis of the cellular RNA using an amylase cDNA probe. Thus the regulation of amylase synthesis in rats maintained on liquid diets may take place at the level of protein translation, as well as of differential mRNA stability or gene transcription.

Amylases↗
PubMed1989

[Analytic measurement of the solubility of the enamel surface exposed to acid and morphometric study of the resulting erosion in rat incisors treated with aluminum].

Their method of examination is based on the area analytical examination of scanning electromicroscopic photographs made of the enamel surfaces corroded with acid. By means of their method the area distribution of the enamel surfaces has been determined on which no detectable changes were formed after the acid action. The results obtained that way have also been compared with the results of analytical measurements. Their examinations were performed on uppar incisors of rats treated with aluminium.

Acid Etching, Dental↗
PubMed1987

Alpha-lactalbumin acts as a bimodal regulator of rat parotid acinar cell growth.

Isoproterenol, a beta-adrenergic receptor agonist, causes hypertrophy and hyperplasia of the rat parotid gland. The stimulation of parotid acinar cells to a growth phase is accompanied by a cell surface localization of the enzyme 4 beta-galactosyltransferase. Alpha-lactalbumin, a specific modifier protein for 4 beta-galactosyltransferase, when given subsequent to the initiation of isoproterenol treatment and the commencement of parotid enlargement, resulted in a termination of gland hypertrophy and DNA synthesis. Gland size did not, however, return to control levels with the continued injection of isoproterenol and alpha- lactalbumin. In contrast, the injection of alpha-lactalbumin in neonatal rats (7-14 days post-partum) stimulated parotid gland hypertrophy and DNA synthesis. This treatment also lead to the precocious expression of the major parotid gland salivary enzyme, amylase.

Age Factors↗