Involvement of prostaglandin E2 derived from enteric glial cells in the action of bradykinin in cultured rat myenteric neurons

Murakami, Matsuka; Ohta, Toshio; Otsuguro, Ken-ichi; S, Itó

doi:10.1016/j.neuroscience.2006.12.052

Cited by 26 publications

(23 citation statements)

References 37 publications

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“…In that study, our group postulated that the long sustaining effect may have involved a slow release of chemical mediators (e.g., PGE 2 or bradykinin) from various cells in the airway mucosa on action of cationic proteins, as discussed above. Although a possible involvement of endogenous autacoids cannot be completely ruled out in the present study because certain potent mediators (e.g., PGE 2 or PGI 2 ) may still be released from isolated neurons or from nonneuronal satellite cells present in the culture (25,39,49), other potential contributing factors should also be considered. For example, it is possible that the sustaining action of MBP is related to cascades of intracellular signaling events triggered by the cationic protein in these neurons (37).…”

Section: Discussionmentioning

confidence: 96%

Sensitization of isolated rat vagal pulmonary sensory neurons by eosinophil-derived cationic proteins

Gu¹,

Wiggers²,

Gleich³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Gu Q, Wiggers ME, Gleich GJ, Lee L-Y. Sensitization of isolated rat vagal pulmonary sensory neurons by eosinophil-derived cationic proteins. Am J Physiol Lung Cell Mol Physiol 294: L544-L552, 2008. First published January 4, 2008 doi:10.1152/ajplung.00271.2007.-It has been shown that airway exposure to eosinophil-derived cationic proteins stimulated vagal pulmonary C fibers and markedly potentiated their responses to lung inflation in anesthetized rats (Lee LY, Gu Q, Gleich GJ, J Appl Physiol 91: 1318 -1326, 2001). However, whether the effects resulted from a direct action of these proteins on the sensory nerves was not known. The present study was therefore carried out to determine the effects of these proteins on isolated rat vagal pulmonary sensory neurons. Our results obtained from perforated whole cell patch-clamp recordings showed that pretreatment with eosinophil major basic protein (MBP; 2 M, 60 s) significantly increased the capsaicin-evoked inward current in these neurons; this effect peaked ϳ10 min after MBP and lasted for Ͼ60 min; in current-clamp mode, MBP substantially increased the number of action potentials evoked by both capsaicin and electrical stimulation. Pretreatment with MBP did not significantly alter the input resistance of these sensory neurons. In addition, the sensitizing effect of MBP was completely abolished when its cationic charge was neutralized by mixing with a polyanion, such as low-molecular-weight heparin or poly-L-glutamic or poly-L-aspartic acid, before its delivery to the neurons. Moreover, a similar sensitizing effect was also generated by other eosinophil granule-derived proteins (e.g., eosinophil peroxidase). These results demonstrate a direct, charge-dependent, and long-lasting sensitizing effect of cationic proteins on pulmonary sensory neurons, which may contribute to the airway hyperresponsiveness associated with airway infiltration of eosinophils under pathophysiological conditions. major basic protein; eosinophil cationic protein; eosinophil peroxidase; airway inflammation; airway hypersensitivity ASTHMA IS CHARACTERIZED BY chronic airway inflammation associated with airway infiltration of various inflammatory cells, particularly the eosinophils (7). Activated eosinophils are known to secrete a number of cationic proteins, including major basic protein (MBP), eosinophil cationic protein (ECP), and eosinophil peroxidase (EPO) (16). Previous studies have shown that intratracheal instillation of eosinophil-derived cationic proteins such as MBP induces bronchoconstriction and bronchial hyperresponsiveness in a number of animal species (9,17,21). Similar effects can also be induced by intratracheal administration of synthetic cationic proteins such as poly-Llysine (PLL) (10,24,46).Most of the sensory inputs arising from airways and lungs are conducted in vagus nerves and their branches. Cell bodies of these sensory nerves reside in two adjacent but distinct anatomic structures, the nodose and intracranial jugular ganglia. It is known that Ͼ75% of vagal bronchopulmonar...

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Section: Discussionmentioning

confidence: 96%

Sensitization of isolated rat vagal pulmonary sensory neurons by eosinophil-derived cationic proteins

Gu¹,

Wiggers²,

Gleich³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…39 Overall, the above and other evidences suggest a close functional link between EGC and enteric neurons. 40 …”

Section: Putative Mechanisms For Egc Influence On Gastrointestinal Momentioning

confidence: 99%

Enteric glial cells: new players in gastrointestinal motility?

Bassotti

Villanacci

Antonelli

et al. 2007

Laboratory Investigation

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The enteric glial cells, in addition to being support structures for the enteric nervous system, have many other additional roles, such as modulators for the homeostasis of enteric neurons, cells involved in enteric neurotransmission and antigenpresenting cells. Moreover, in the last years, data have been accumulating that demonstrate a possible active role of these cells in the pathophysiology of gastrointestinal motor activity. Thus, as also shown by recent evidence in both experimental animal models, and in some human diseases, alterations of enteric glial cells might have some role in the development of intestinal motor abnormalities.

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“…Most, if not all, of these receptors belong to the G-protein-coupled receptor (GPCR) superfamily. Likewise, enteric glia express receptors for bioactive lipids such as the sphingosine-1-phosphate receptor (SP1R) (Segura et al, 2004b) and lysophosphatidic acid receptor 1 (LPA1) (Segura et al, 2004a), endothelin (likely ETB receptors) (Zhang et al, 1997), protease-activate receptors (PAR1 and PAR2) (Garrido et al, 2002) and bradykinin (B2 receptors) (Murakami et al, 2007) but the significance of these receptor types on enteric glia is largely unknown. At present, enteric glia are know to express receptors for adenosine diphosphate (ADP; P2Y1 receptor) (Gomes et al, 2009;McClain et al, 2014), adenosine triphosphate (ATP) and uridine triphosphate (UTP) (both via P2Y4 receptors) (Kimball and Mulholland, 1996;Van Nassauw et al, 2006;Gulbransen and Sharkey, 2009) and adenosine (A2B receptors) (Christofi et al, 2001;Vieira et al, 2011).…”

Section: Receptorsmentioning

confidence: 99%

“…Like NO, prostaglandins produced by enteric glia such as prostaglandin E(2) (PGE2) may serve diverse roles (Murakami et al, 2007). Glial-derived PGE2 may act to modulate enteric neurotransmission, as a vasodilator or as a contributor to oxidative stressor in disease but the role of this compound in the intact ENS is currently unknown.…”

Section: Releasable Factorsmentioning

confidence: 99%

Enteric Glia

Gulbransen¹

2014

Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease

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Involvement of prostaglandin E2 derived from enteric glial cells in the action of bradykinin in cultured rat myenteric neurons

Cited by 26 publications

References 37 publications

Sensitization of isolated rat vagal pulmonary sensory neurons by eosinophil-derived cationic proteins

Sensitization of isolated rat vagal pulmonary sensory neurons by eosinophil-derived cationic proteins

Enteric glial cells: new players in gastrointestinal motility?

Enteric Glia

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