Modulation of Intracellular Second Messengers by Dietary Fat during Colonic Tumor Development

1997 ◽  
pp. 85-96 ◽  
Author(s):  
Robert S. Chapkin ◽  
Yi-Hai Jiang ◽  
Laurie A. Davidson ◽  
Joanne R. Lupton
Keyword(s):  
Dietary Fat ◽  
Second Messengers ◽  
Tumor Development ◽  
Colonic Tumor ◽  
Intracellular Second Messengers

scholarly journals Dietary fat and fiber differentially alter intracellular second messengers during tumor devolopment in rat colon

1996 ◽  
Vol 17 (6) ◽  
pp. 1227-1233 ◽  
Author(s):  
Yi-Hai Jiang ◽  
Joanne R. Lupton ◽  
Wen-chi L. Chang ◽  
Christopher A. Jolly ◽  
Harold M. Aukema ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Second Messengers ◽  
Rat Colon ◽  
Intracellular Second Messengers

Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels

1998 ◽  
Vol 78 (1) ◽  
pp. 53-97 ◽  
Author(s):  
FRANK M. FARACI ◽  
DONALD D. HEISTAD
Keyword(s):  
Potassium Channels ◽  
Cerebral Circulation ◽  
Second Messengers ◽  
Chronic Hypertension ◽  
Major Mechanism ◽  
Disease States ◽  
Vasoactive Factors ◽  
New Concepts ◽  
Intracellular Second Messengers

Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.

PACAP38 Modulates Activity of NMDA Receptors in Cultured Chick Cortical Neurons

1997 ◽  
Vol 78 (4) ◽  
pp. 2231-2234 ◽  
Author(s):  
Guo Jun Liu ◽  
Barry W. Madsen
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Cortical Neurons ◽  
Second Messengers ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Low Concentrations ◽  
Channel Opening ◽  
Pituitary Adenylate Cyclase ◽  
Intracellular Second Messengers

Liu, Guo Jun and Barry W. Madsen. PACAP38 modulates activity of NMDA receptors in cultured chick cortical neurons. J. Neurophysiol. 78: 2231–2234, 1997. The outside-out recording mode of the patch-clamp technique was used to study modulatory effects of pituitary adenylate cyclase-activating polypeptide (PACAP38) on N-methyl-d-aspartate (NMDA) receptor activity in cultured chick cortical neurons. Biphasic concentration-dependent effects of PACAP38 on channel opening frequency induced by NMDA (20 μM) and glycine (1 μM) were found, with low concentrations (0.5–2 nM) of PACAP38 increasing activity and higher concentrations (10–1,000 nM) causing inhibition. These effects were reversible, reduced with higher concentrations of glycine (2–10 μM) but not by 200 μM NMDA, and inhibited by 10 μM 7-chlorokynurenic acid. In addition, 1 μM PACAP6–38 (a PACAP antagonist) inhibited channel activity due to 20 μM NMDA and 1 μM glycine by 66%, and this inhibition was reduced to 13% in the additional presence of 2 nM PACAP38. These observations suggest thatPACAP38 has a direct modulatory effect on the NMDA receptor that is independent of intracellular second messengers and probably mediated through the glycine coagonist site(s).

scholarly journals Dietary Iron Enhances Colonic Inflammation and IL-6/IL-11-Stat3 Signaling Promoting Colonic Tumor Development in Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e78850 ◽  
Author(s):  
Anita C. G. Chua ◽  
Borut R. S. Klopcic ◽  
Desiree S. Ho ◽  
S. Kristine Fu ◽  
Cynthia H. Forrest ◽  
...  
Keyword(s):  
Tumor Development ◽  
Dietary Iron ◽  
Colonic Inflammation ◽  
Colonic Tumor ◽  
Stat3 Signaling

Arachidonic acid inhibits potassium conductances in cultured rat oligodendrocytes

1995 ◽  
Vol 269 (2) ◽  
pp. C341-C348 ◽  
Author(s):  
B. Soliven ◽  
N. Wang
Keyword(s):  
Arachidonic Acid ◽  
Second Messengers ◽  
Membrane Depolarization ◽  
Patch Clamp Technique ◽  
Metabolic Products ◽  
Potassium Conductances ◽  
K Current ◽  
Intracellular Second Messengers ◽  
Inwardly Rectifying ◽  
K Currents

Arachidonic acid (AA) and its metabolites play a dual role as intracellular second messengers and as transcellular mediators of neural activity. We have previously shown that AA increases cytosolic Ca2+ in oligodendrocytes. In this work, we studied the effects of AA and other fatty acids on whole cell K+ currents of cultured rat oligodendrocytes using the patch-clamp technique. We found that 1) AA decreased the current amplitudes of both the inwardly rectifying K+ current (IKir) and the outward K+ currents (IKo) resulting in membrane depolarization; 2) AA also induced IKo current inactivation/blocked state; 3) AA appeared to act directly on K+ channels and not indirectly via its metabolic products, activation of protein kinase C, or by generation of oxygen free radicals. We have thus demonstrated an additional mechanism for AA-induced signaling in oligodendrocytes, i.e., via modulation of K+ conductances leading to membrane depolarization. The latter has been shown to influence protein phosphorylation and perhaps other important functional output of oligodendrocytes.

Adenine nucleotides as paracrine mediators and intracellular second messengers in immunity and inflammation

2019 ◽  
Vol 47 (1) ◽  
pp. 329-337 ◽  
Author(s):  
Ralf Fliegert ◽  
Jörg Heeren ◽  
Friedrich Koch-Nolte ◽  
Viacheslav O. Nikolaev ◽  
Christian Lohr ◽  
...  
Keyword(s):  
Immune System ◽  
T Lymphocytes ◽  
Immune Responses ◽  
Nicotinamide Adenine Dinucleotide ◽  
Adenine Nucleotides ◽  
Second Messengers ◽  
Cellular Responses ◽  
Fine Tuning ◽  
Inflammatory Processes ◽  
Intracellular Second Messengers

Abstract Adenine nucleotides (AdNs) play important roles in immunity and inflammation. Extracellular AdNs, such as adenosine triphosphate (ATP) or nicotinamide adenine dinucleotide (NAD) and their metabolites, act as paracrine messengers by fine-tuning both pro- and anti-inflammatory processes. Moreover, intracellular AdNs derived from ATP or NAD play important roles in many cells of the immune system, including T lymphocytes, macrophages, neutrophils and others. These intracellular AdNs are signaling molecules that transduce incoming signals into meaningful cellular responses, e.g. activation of immune responses against pathogens.

scholarly journals Generation and characterization of a lysosomally targeted, genetically encoded Ca2+-sensor

2012 ◽  
Vol 449 (2) ◽  
pp. 449-457 ◽  
Author(s):  
Hannah V. McCue ◽  
Joanna D. Wardyn ◽  
Robert D. Burgoyne ◽  
Lee P. Haynes
Keyword(s):  
Second Messengers ◽  
Eukaryotic Cell ◽  
Endocytic Pathway ◽  
Cell Physiology ◽  
Simple Method ◽  
Late Endosomes ◽  
Intracellular Organelles ◽  
Intracellular Second Messengers ◽  
The Impact

Distinct spatiotemporal Ca2+ signalling events regulate fundamental aspects of eukaryotic cell physiology. Complex Ca2+ signals can be driven by release of Ca2+ from intracellular organelles that sequester Ca2+ such as the ER (endoplasmic reticulum) or through the opening of Ca2+-permeable channels in the plasma membrane and influx of extracellular Ca2+. Late endocytic pathway compartments including late-endosomes and lysosomes have recently been observed to sequester Ca2+ to levels comparable with those found within the ER lumen. These organelles harbour ligand-gated Ca2+-release channels and evidence indicates that they can operate as Ca2+-signalling platforms. Lysosomes sequester Ca2+ to a greater extent than any other endocytic compartment, and signalling from this organelle has been postulated to provide ‘trigger’ release events that can subsequently elicit more extensive Ca2+ signals from stores including the ER. In order to investigate lysosomal-specific Ca2+ signalling a simple method for measuring lysosomal Ca2+ release is essential. In the present study we describe the generation and characterization of a genetically encoded, lysosomally targeted, cameleon sensor which is capable of registering specific Ca2+ release in response to extracellular agonists and intracellular second messengers. This probe represents a novel tool that will permit detailed investigations examining the impact of lysosomal Ca2+ handling on cellular physiology.

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