Gαq signalling: The new and the old

Sánchez-Fernández, Guzmán; Cabezudo, Sofía; García-Hoz, Carlota; Benincá, Cristiane; Aragay, Anna M.; Mayor, Federico; Ribas, Catalina

doi:10.1016/j.cellsig.2014.01.010

Cited by 85 publications

(82 citation statements)

References 222 publications

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“…Other factors, like the stress associated with labor and blood acidemia, should also be considered. Both adrenergic stimulation and extracellular acidosis has been shown to interfere with G αq -dependent cellular activities and neutrophil functions (28,29). Neutrophils represent a highly heterogeneous cell population.…”

Section: Discussionmentioning

confidence: 99%

Effects of local anesthetics on the respiratory burst of cord blood neutrophils in vitro

et al. 2016

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Background: Whether local anesthetics exert anti-inflammatory effects in fetal and newborn systemic neutrophils is unclear. The aim of the present study was to assess the effects of bupivacaine and lidocaine on the respiratory burst of cord blood neutrophils in vitro compared with adult cells. Methods: Whole cord blood (n = 12) and control adult blood samples (n = 7) were incubated with bupivacaine (0.0005, 0.005, 0.05, 1 mmol/l) and lidocaine (0.002, 0.02, 0.2, 4 mmol/l) for 1 and 4 h. The production of reactive oxygen species (ROS) by unstimulated neutrophils and the phorbol myristate acetate-induced oxidative burst were assessed by flow cytometry. A subset of neutrophils showing high fluorescence intensity (rho+) was analyzed separately. results: After 1 h incubation, local anesthetics decreased the respiratory burst in whole cord blood and adult neutrophils in a similar manner. At the clinically relevant concentration of 0.0005 mmol/l, bupivacaine was active, but its effect in cord blood cells could not be detected after 4 h. The cord blood rho+ cell subset was unresponsive to the inhibitory action of bupivacaine. In rho+ neutrophils, basal ROS production was stimulated by lidocaine at the lowest concentration tested. conclusion: Bupivacaine and lidocaine can decrease the respiratory burst in neutrophils of term newborns. t he question of the effects of local anesthetics (LAs) on fetal neutrophils arises in the clinical context of the broad application of neuraxial blockade in obstetrics. Epidural technics are the gold standard for labor intrapartum analgesia and are administered to parturients on request. By applying higher doses of LAs through the existing epidural catheter, surgical anesthesia for cesarean delivery may be easily obtained. The fetal and neonatal implications of epidural techniques are mostly considered to be indirect and dependent on modulation of maternal physiology, and are associated with a higher risk of neonatal pyrexia and sepsis evaluation, but not neonatal infection (1-3). The reasons for these findings are not sufficiently clear. However, direct fetal and neonatal effects of LAs as a result of placental drug transfer should not be entirely excluded. LAs administered epidurally enter the maternal systemic circulation and, after crossing the placental barrier, can reach the fetal circulation, with levels approximately one-third to half those seen in the maternal circulation. Furthermore, because of ion trapping and slower elimination, LAs may persist for longer in fetal and neonatal than maternal blood (4). LAs in the fetal systemic circulation have been reported to abolish an offspring's cardiovascular adaptive reaction to asphyxia (5) and have been suggested to affect blood cells. Specifically, bupivacaine has been shown to modify plasma membrane properties of fetal erythrocytes (6). In other studies, lidocaine, a prototypical amino-amide agent administered epidurally for cesarean sections, was suggested to be responsible for the inhibition of natural killer cells and neutrophil a...

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Section: Discussionmentioning

confidence: 99%

Effects of local anesthetics on the respiratory burst of cord blood neutrophils in vitro

et al. 2016

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“…Most of them may have a high guanosine triphosphatase activating protein (GAP) activity, but not PI-PLC ␤ 1, that can also be regulated by a distinct binding region to phosphatidic acid or is specifi cally activated by MAPK, therefore playing important roles in cell metabolism (19)(20)(21)(22)(23). Upon PI-PLC ␤ 1 activation in the nucleus, IP3 generation occurs ( Fig.…”

Section: Function and Regulationmentioning

confidence: 99%

Phosphoinositide-specific phospholipase C in health and disease

Cocco

Follo

Manzoli

et al. 2015

Journal of Lipid Research

140

100

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“…IP 3 can go on to increase intracellular Ca 2+ , which along with DAG can bind and activate protein kinase C (Figure 3; reviewed by Sánchez-Fernández et al, 2014: PMID 24440667). Prior to studies of Gα q signaling in C. elegans , the only confirmed direct Gα q effector was PLCβ.…”

Section: The Mechanism Of Signaling By Neural Heterotrimeric G Promentioning

confidence: 99%

Neurotransmitter signaling through heterotrimeric G proteins: insights from studies in C. elegans

Koelle

2018

WormBook

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Neurotransmitters signal via G protein coupled receptors (GPCRs) to modulate activity of neurons and muscles. C. elegans has ~150 G protein coupled neuropeptide receptor homologs and 28 additional GPCRs for small-molecule neurotransmitters. Genetic studies in C. elegans demonstrate that neurotransmitters diffuse far from their release sites to activate GPCRs on distant cells. Individual receptor types are expressed on limited numbers of cells and thus can provide very specific regulation of an individual neural circuit and behavior. G protein coupled neurotransmitter receptors signal principally via the three types of heterotrimeric G proteins defined by the G alpha subunits Gαo, Gαq, and Gαs. Each of these G alpha proteins is found in all neurons plus some muscles. Gαo and Gαq signaling inhibit and activate neurotransmitter release, respectively. Gαs signaling, like Gαq signaling, promotes neurotransmitter release. Many details of the signaling mechanisms downstream of Gαq and Gαs have been delineated and are consistent with those of their mammalian orthologs. The details of the signaling mechanism downstream of Gαo remain a mystery. Forward genetic screens in C. elegans have identified new molecular components of neural G protein signaling mechanisms, including Regulators of G protein Signaling (RGS proteins) that inhibit signaling, a new Gαq effector (the Trio RhoGEF domain), and the RIC-8 protein that is required for neuronal Gα signaling. A model is presented in which G proteins sum up the variety of neuromodulator signals that impinge on a neuron to calculate its appropriate output level.

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Gαq signalling: The new and the old

Cited by 85 publications

References 222 publications

Effects of local anesthetics on the respiratory burst of cord blood neutrophils in vitro

Effects of local anesthetics on the respiratory burst of cord blood neutrophils in vitro

Phosphoinositide-specific phospholipase C in health and disease

Neurotransmitter signaling through heterotrimeric G proteins: insights from studies in C. elegans

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