Vasoactive intestinal peptide increases intracellular cAMP and gonadotropin-alpha gene activity in JEG-3 syncytial trophoblasts. Constraints posed by desensitization.

Although vasoactive intestinal peptide (VIP) has been postulated to function in modulation of T cell trafficking, the exact mechanism has not been elucidated in vivo. In the present study, the effects of VIP on T lymphocyte migration were examined in rat Peyer's patches. T lymphocytes collected from intestinal lymph of rats were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein. Peyer's patches of the recipient rats were observed with intravital fluorescence microscopy. In vivo intra-arterial infusion of or in vitro incubation with VIP did not affect the initial lymphocyte interaction with postcapillary venules of Peyer's patches. However, these treatments with VIP significantly inhibited transendothelial migration and also significantly blocked the interstitial migration of T cells and inhibited their subsequent appearance in the interfollicular lymphatics. Treatment with adenosine 3',5'-cyclic monophosphate (cAMP)-inducing agents resulted in similar inhibitory effect on T lymphocyte migration in Peyer's patches. In conclusion, VIP has significant inhibitory effects on T lymphocyte migration in Peyer's patches, possibly mediated by elevation of the intracellular cAMP concentrations.

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Physiological cAMP-elevating secretagogues differentially regulate fluid and protein secretions in mouse submandibular and sublingual glands

AJP Cell Physiology ◽

10.1152/ajpcell.00421.2018 ◽

2019 ◽

Vol 316 (5) ◽

pp. C690-C697 ◽

Cited By ~ 1

Author(s):

Yusuke Kondo ◽

James E. Melvin ◽

Marcelo A. Catalan

Keyword(s):

Vasoactive Intestinal Peptide ◽

Ex Vivo ◽

Sympathetic Innervation ◽

Fluid Secretion ◽

Intracellular Camp ◽

Functional Differences ◽

Parasympathetic Regulation ◽

G Protein Coupled ◽

Dependent Pathway ◽

Sympathetic And Parasympathetic Regulation

The mechanisms underlying the functional differences in sympathetic and parasympathetic regulation of the major salivary glands have received little attention. The acute effects of parasympathetic muscarinic (carbachol)-dependent and combined parasympathetic-dependent plus cAMP-dependent pathways on fluid secretion rates, ion composition, and protein content were assessed using a newly developed ex vivo preparation that allows the simultaneous perfusion of the mouse submandibular (SMGs) and sublingual glands (SLGs). Our results confirm that the muscarinic-dependent pathway accounts for the bulk of salivation in SMGs and SLGs, whereas costimulation with a cAMP-increasing agent (forskolin, isoproterenol, or vasoactive intestinal peptide) did not increase the flow rate. Costimulation with carbachol plus the β-adrenergic agonist isoproterenol decreased the concentration of NaCl and produced a substantial increase in the protein and Ca2+ content of SMG but not SLG saliva, consistent with a sparse sympathetic innervation of the SLGs. On the other hand, forskolin, which bypasses receptors to increase intracellular cAMP by directly activating the enzyme adenylate cyclase, enhanced the secretion of protein and Ca2+ by both the SMGs and SLGs. In contrast, isoproterenol and vasoactive intestinal peptide specifically stimulated protein secretion in SMG and SLG salivas, respectively. In summary, cAMP-dependent signaling does not play a major role in the stimulation of fluid secretion in SMGs and SLGs, whereas each cAMP-increasing agonist behaves differently in a gland-specific manner suggesting differential expression of G protein-coupled receptors in the epithelial cells of SMGs and SLGs.

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Introduction

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100070266 ◽

1978 ◽

Vol 36 (3) ◽

pp. 543-544

Author(s):

W. Bernard

Keyword(s):

Molecular Weight ◽

Electron Microscope ◽

Nucleic Acid ◽

Gene Mapping ◽

Molecular Genetics ◽

Cell Biology ◽

Gene Activity ◽

Close Connection ◽

Basic Information ◽

Simple Systems

In comparison to many other fields of ultrastructural research in Cell Biology, the successful exploration of genes and gene activity with the electron microscope in higher organisms is a late conquest. Nucleic acid molecules of Prokaryotes could be successfully visualized already since the early sixties, thanks to the Kleinschmidt spreading technique - and much basic information was obtained concerning the shape, length, molecular weight of viral, mitochondrial and chloroplast nucleic acid. Later, additonal methods revealed denaturation profiles, distinction between single and double strandedness and the use of heteroduplexes-led to gene mapping of relatively simple systems carried out in close connection with other methods of molecular genetics.

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Chronic interferon- α treatment leads to adaptations of opioid receptors-mediated intracellular cAMP pathway in human neuroblastoma SK-N-SH cells

Neuroscience Research ◽

10.1016/s0168-0102(00)81596-5 ◽

2000 ◽

Vol 38 ◽

pp. S125

Author(s):

N Nishiyama

Keyword(s):

Opioid Receptors ◽

Interferon Α ◽

Intracellular Camp ◽

Human Neuroblastoma ◽

Camp Pathway

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Transmembrane Calcium Influx Associated with von Willebrand Factor Binding to GP Ib in the Initiation of Shear-Induced Platelet Aggregation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651640 ◽

1993 ◽

Vol 69 (05) ◽

pp. 496-502 ◽

Cited By ~ 123

Author(s):

Yasuo Ikeda ◽

Makoto Handa ◽

Tetsuji Kamata ◽

Koichi Kawano ◽

Yohko Kawai ◽

...

Keyword(s):

Shear Force ◽

Calcium Influx ◽

Fold Increase ◽

Intracellular Camp ◽

Recombinant Fragment ◽

Transmembrane Flux ◽

Irreversible Aggregation ◽

Von Willebrand ◽

Willebrand Factor ◽

Camp Levels

SummaryWe found that the binding of multimeric vWF to GP Ib under a shear force of 108 dynes/cm2 resulted in the transmembrane flux of Ca2+ ions with a two-to three-fold increase in their intracellular concentration ([Ca2+]i). The blockage of this event, obtained by inhibiting the vWF-GP Ib interaction, suppressed aggregation. In contrast, the blockage of vWF binding to GP IIb-IIIa, as well as the prevention of activation caused by increased intracellular cAMP levels, inhibited aggregation but had no significant effect on [Ca2+]i increase. A monomeric recombinant fragment of vWF containing the GP Ib-binding domain of the molecule (residues 445-733) prevented all effects mediated by multimeric vWF but, by itself, failed to support the increase in [Ca2+]i and aggregation. These results suggest that the binding of multimeric vWF to GP Ib initiates platelets aggregation induced by high shear stress by mediating a transmembrane flux of Ca2+ ions, perhaps through a receptor-dependent calcium channel. The increase in [Ca2+]i may act as an intracellular message and cause the activation of GP IIb-IIIa; the latter receptor then binds vWF and mediates irreversible aggregation.

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Effect of Cyclic AMP and Cyclic GMP on Thromboplastin (Factor III) Synthesis in Human Monocytes In Vitro

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665317 ◽

1983 ◽

Vol 50 (04) ◽

pp. 804-809 ◽

Cited By ~ 16

Author(s):

Torstein Lyberg

Keyword(s):

Cyclic Amp ◽

Cyclic Gmp ◽

Immune Complexes ◽

Phosphodiesterase Inhibitors ◽

Inhibitory Effect ◽

Intracellular Camp ◽

Human Monocytes ◽

Purified Protein Derivative ◽

A 23187

SummaryHuman monocytes in vitro respond to various agents (immune complexes, lectins, endotoxin, the divalent ionophore A 23187, 12-0-tetradecanoyl-phorbol 13-acetate [TPA], purified protein derivative [PPD] of Bacille Calmette-Guerin) with an increased synthesis of the protein component of thromboplastin. The effect of cyclic AMP and cyclic GMP on this response has been studied. Dibutyryl-cyclic AMP, prostaglandin E1 and the phosphodiesterase inhibitors 3-butyl-1-methyl-xanthine (MIX) and rac -4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 201724), separately and in combination have a pronounced inhibitory effect on the response to immune complexes and PPD, and a moderate effect on the response to endotoxin and lectins. The effect on TPA response and on the response to A 23187 was slight. Dibutyryl-cyclic GMP (1 mM) gave a slight inhibition of the TPA arid IC response, but had essentially no effect on the response to other inducers. The intracellular cAMP level increased when monocytes were incubated with IC, TPA or A 23187 followed by a decrease to basal levels within 1-2 hr, whereas lectin (PHA) and PPD did not induce such changes. The cAMP response to endotoxin varied. Stimulation with IC induced an increase in monocyte cGMP levels, whereas the other stimulants did not cause such changes.

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