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Article ; Online: Inflammation without pain: Immune-derived opioids hold the key.

Carbone, Simona E / Poole, Daniel P

Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society

2020 Volume 32, Issue 2, Page(s) e13787

Abstract: Visceral pain is commonly associated with acute or remitting inflammatory bowel disease (IBD). In marked contrast, chronic IBD is often painless, even in the presence of active inflammation. This suggests that inflammation in itself is insufficient to ... ...

Abstract	Visceral pain is commonly associated with acute or remitting inflammatory bowel disease (IBD). In marked contrast, chronic IBD is often painless, even in the presence of active inflammation. This suggests that inflammation in itself is insufficient to sustain altered nociceptive signaling and raises the possibility that there is an endogenous analgesic system in effect in chronic disease. A new study by Basso et al. published in this issue of Neurogastroenterology & Motility provides additional support for an immune-mediated mechanism that suppresses visceral hypersensitivity. The authors examined visceral pain in the IL-10-piroxicam model of chronic colitis, which differs from other experimental IBD models in that it involves immune suppression. During active inflammation, responses by these mice to graded increases in colorectal distension were equivalent to healthy controls, consistent with normal afferent signaling. However, treatment with a peripherally restricted opioid receptor antagonist resulted in marked visceral hypersensitivity to the same stimuli. This effect was attributed to the production of endogenous opioids by colitogenic CD4
MeSH term(s)	Animals ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/metabolism ; Opioid Peptides/metabolism ; Pain/immunology ; Pain/metabolism
Chemical Substances	Opioid Peptides
Language	English
Publishing date	2020-04-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1186328-6
ISSN	1365-2982 ; 1350-1925
ISSN (online)	1365-2982
ISSN	1350-1925
DOI	10.1111/nmo.13787
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Article ; Online: Diverse Roles of TRPV4 in Macrophages: A Need for Unbiased Profiling.

Nguyen, Thanh-Nhan / Siddiqui, Ghizal / Veldhuis, Nicholas A / Poole, Daniel P

Frontiers in immunology

2022 Volume 12, Page(s) 828115

Abstract: Transient receptor potential vanilloid 4 (TRPV4) is a non-selective mechanosensitive ion channel expressed by various macrophage populations. Recent reports have characterized the role of TRPV4 in shaping the activity and phenotype of macrophages to ... ...

Abstract	Transient receptor potential vanilloid 4 (TRPV4) is a non-selective mechanosensitive ion channel expressed by various macrophage populations. Recent reports have characterized the role of TRPV4 in shaping the activity and phenotype of macrophages to influence the innate immune response to pathogen exposure and inflammation. TRPV4 has been studied extensively in the context of inflammation and inflammatory pain. Although TRPV4 activity has been generally described as pro-inflammatory, emerging evidence suggests a more complex role where this channel may also contribute to anti-inflammatory activities. However, detailed understanding of how TRPV4 may influence the initiation, maintenance, and resolution of inflammatory disease remains limited. This review highlights recent insights into the cellular processes through which TRPV4 contributes to pathological conditions and immune processes, with a focus on macrophage biology. The potential use of high-throughput and omics methods as an unbiased approach for studying the functional outcomes of TRPV4 activation is also discussed.
MeSH term(s)	Animals ; Carrier Proteins ; Disease Management ; Disease Susceptibility ; Energy Metabolism ; Gene Expression Regulation ; Humans ; Ligands ; Macrophage Activation/genetics ; Macrophage Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Mechanotransduction, Cellular ; Molecular Targeted Therapy ; Protein Binding ; Signal Transduction ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism
Chemical Substances	Carrier Proteins ; Ligands ; TRPV Cation Channels ; TRPV4 protein, human
Language	English
Publishing date	2022-01-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.828115
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Article ; Online: Mini-review: Dissecting receptor-mediated stimulation of TRPV4 in nociceptive and inflammatory pathways.

Peng, Scott / Poole, Daniel P / Veldhuis, Nicholas A

Neuroscience letters

2021 Volume 770, Page(s) 136377

Abstract: Transient Receptor Potential Vanilloid 4 (TRPV4) is a polymodal, non-selective cation channel that detects thermal, mechanical, and environmental cues and contributes to a range of diverse physiological processes. The effects of chronic TRPV4 stimulation ...

Abstract	Transient Receptor Potential Vanilloid 4 (TRPV4) is a polymodal, non-selective cation channel that detects thermal, mechanical, and environmental cues and contributes to a range of diverse physiological processes. The effects of chronic TRPV4 stimulation and gain-of-function genetic mutations suggest that TRPV4 may also be a valuable therapeutic target for pathophysiological events including neurogenic inflammation, peripheral neuropathies, and impaired wound healing. There has been significant interest in defining how and where TRPV4 may promote inflammation and pain. Endogenous stimuli such as osmotic stress and lipid binding are established TRPV4 activators. The TRP channel family is also well-known to be controlled by 'receptor-operated' pathways. For example, G protein-coupled receptors (GPCRs) expressed by primary afferent neurons or other cells in inflammatory pathways utilize TRPV4 as an effector protein to amplify nociceptive and inflammatory signaling. Contributing to disorders including arthritis, neuropathies, and pulmonary edema, GPCRs such as the protease-activated receptor PAR2 mediate activation of kinase signaling cascades to increase TRPV4 phosphorylation, resulting in sensitization and enhanced neuronal excitability. Phospholipase activity also leads to production of polyunsaturated fatty acid lipid mediators that directly activate TRPV4. Consistent with the contribution of TRPV4 to disease, pharmacological inhibition or genetic ablation of TRPV4 can diminish receptor-mediated inflammatory events. This review outlines how receptor-mediated signaling is a major endogenous driver of TRPV4 gating and discusses key signaling pathways and emerging TRPV4 modulators such as the mechanosensitive Piezo1 ion channel. A collective understanding of how endogenous stimuli can influence TRPV4 function is critical for future therapeutic endeavors to modulate this channel.
MeSH term(s)	Animals ; Humans ; Neurogenic Inflammation/metabolism ; Nociception ; Signal Transduction ; TRPV Cation Channels/metabolism
Chemical Substances	TRPV Cation Channels ; TRPV4 protein, human
Language	English
Publishing date	2021-11-29
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2021.136377
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Article ; Online: Therapeutic potential of allosteric modulators for the treatment of gastrointestinal motility disorders.

Saito, Ayame / Alvi, Sadia / Valant, Celine / Christopoulos, Arthur / Carbone, Simona E / Poole, Daniel P

British journal of pharmacology

2022

Abstract: Gastrointestinal motility is tightly regulated by the enteric nervous system (ENS). Disruption of coordinated enteric nervous system activity can result in dysmotility. Pharmacological treatment options for dysmotility include targeting of G protein- ... ...

Abstract	Gastrointestinal motility is tightly regulated by the enteric nervous system (ENS). Disruption of coordinated enteric nervous system activity can result in dysmotility. Pharmacological treatment options for dysmotility include targeting of G protein-coupled receptors (GPCRs) expressed by neurons of the enteric nervous system. Current GPCR-targeting drugs for motility disorders bind to the highly conserved endogenous ligand-binding site and promote indiscriminate activation or inhibition of the target receptor throughout the body. This can be associated with significant side-effect liability and a loss of physiological tone. Allosteric modulators of GPCRs bind to a distinct site from the endogenous ligand, which is typically less conserved across multiple receptor subtypes and can modulate endogenous ligand signalling. Allosteric modulation of GPCRs that are important for enteric nervous system function may provide effective relief from motility disorders while limiting side-effects. This review will focus on how allosteric modulators of GPCRs may influence gastrointestinal motility, using 5-hydroxytryptamine (5-HT), acetylcholine (ACh) and opioid receptors as examples.
Language	English
Publishing date	2022-12-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.16023
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Article ; Online: Stroke Alters the Function of Enteric Neurons to Impair Smooth Muscle Relaxation and Dysregulates Gut Transit.

Kumar, Kathryn Prame / Wilson, Jenny L / Nguyen, Huynh / McKay, Liam D / Wen, Shu Wen / Sepehrizadeh, Tara / de Veer, Michael / Rajasekhar, Pradeep / Carbone, Simona E / Hickey, Michael J / Poole, Daniel P / Wong, Connie H Y

Journal of the American Heart Association

2024 Volume 13, Issue 3, Page(s) e033279

Abstract: Background: Gut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of ...

Abstract	Background: Gut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of muscle cells in the gut wall. More recently, studies of gut inflammation revealed interactions of macrophages with enteric neurons are also involved in modulating gut motility. However, whether poststroke gut dysmotility is mediated by direct signaling to the enteric nervous system or indirectly via inflammatory macrophages is unknown. Methods and results: We examined these hypotheses by using a clinically relevant permanent intraluminal midcerebral artery occlusion experimental model of stroke. At 24 hours after stroke, we performed in vivo and ex vivo gut motility assays, flow cytometry, immunofluorescence, and transcriptomic analysis. Stroke-induced gut dysmotility was associated with recruitment of muscularis macrophages into the gastrointestinal tract and redistribution of muscularis macrophages away from myenteric ganglia. The permanent intraluminal midcerebral artery occlusion model caused changes in gene expression in muscularis macrophages consistent with an altered phenotype. While the size of myenteric ganglia after stroke was not altered, myenteric neurons from post-permanent intraluminal midcerebral artery occlusion mice showed a reduction in neuronal nitric oxide synthase expression, and this response was associated with enhanced intestinal smooth muscle contraction ex vivo. Finally, chemical sympathectomy with 6-hydroxydopamine prevented the loss of myenteric neuronal nitric oxide synthase expression and stroke-induced slowed gut transit. Conclusions: Our findings demonstrate that activation of the sympathetic nervous system after stroke is associated with reduced neuronal nitric oxide synthase expression in myenteric neurons, resulting in impaired smooth muscle relaxation and dysregulation of gut transit.
MeSH term(s)	Mice ; Animals ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Enteric Nervous System/metabolism ; Neurons/physiology ; Muscle Relaxation ; Stroke/metabolism
Chemical Substances	Nitric Oxide Synthase Type I (EC 1.14.13.39)
Language	English
Publishing date	2024-01-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.033279
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Article ; Online: New small molecule fluorescent probes for G protein-coupled receptors: valuable tools for drug discovery.

Conner, Joshua W / Poole, Daniel P / Jörg, Manuela / Veldhuis, Nicholas A

Future medicinal chemistry

2020 Volume 13, Issue 1, Page(s) 63–90

Abstract: G protein-coupled receptors (GPCRs) are essential signaling proteins and tractable therapeutic targets. To develop new drug candidates, GPCR drug discovery programs require versatile, sensitive pharmacological tools for ligand binding and compound ... ...

Abstract	G protein-coupled receptors (GPCRs) are essential signaling proteins and tractable therapeutic targets. To develop new drug candidates, GPCR drug discovery programs require versatile, sensitive pharmacological tools for ligand binding and compound screening. With the availability of new imaging modalities and proximity-based ligand binding technologies, fluorescent ligands offer many advantages and are increasingly being used, yet labeling small molecules remains considerably more challenging relative to peptides. Focusing on recent fluorescent small molecule studies for family A GPCRs, this review addresses some of the key challenges, synthesis approaches and structure-activity relationship considerations, and discusses advantages of using high-resolution GPCR structures to inform conjugation strategies. While no single approach guarantees successful labeling without loss of affinity or selectivity, the choice of fluorophore, linker type and site of attachment have proved to be critical factors that can significantly affect their utility in drug discovery programs, and as discussed, can sometimes lead to very unexpected results.
MeSH term(s)	Amino Acid Sequence ; Binding Sites ; Buprenorphine/chemistry ; Buprenorphine/metabolism ; Crystallization ; Drug Evaluation, Preclinical ; Fatty Acids/chemistry ; Fatty Acids/metabolism ; Fluorescence Resonance Energy Transfer ; Fluorescent Dyes/chemistry ; Humans ; Ligands ; Morphine/chemistry ; Morphine/metabolism ; Optical Imaging ; Oxytocin/chemistry ; Oxytocin/metabolism ; Protein Binding ; Protein Conformation ; Receptors, G-Protein-Coupled/chemistry ; Receptors, G-Protein-Coupled/metabolism ; Structure-Activity Relationship
Chemical Substances	Fatty Acids ; Fluorescent Dyes ; Ligands ; Receptors, G-Protein-Coupled ; Buprenorphine (40D3SCR4GZ) ; Oxytocin (50-56-6) ; Morphine (76I7G6D29C)
Language	English
Publishing date	2020-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc-2019-0327
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Article: G Protein-Coupled Receptor Trafficking and Signalling in the Enteric Nervous System: The Past, Present and Future.

Poole, Daniel P / Bunnett, Nigel W

Advances in experimental medicine and biology

2016 Volume 891, Page(s) 145–152

Abstract: G protein-coupled receptors (GPCRs) enable cells to detect and respond to changes in their extracellular environment. With over 800 members, the GPCR family includes receptors for a diverse range of agonists including olfactants, neurotransmitters and ... ...

Abstract	G protein-coupled receptors (GPCRs) enable cells to detect and respond to changes in their extracellular environment. With over 800 members, the GPCR family includes receptors for a diverse range of agonists including olfactants, neurotransmitters and hormones. Importantly, GPCRs represent a major therapeutic target, with approximately 50 % of all current drugs acting at some aspect of GPCR signalling (Audet and Bouvier 2008). GPCRs are widely expressed by all cell types in the gastrointestinal (GI) tract and are major regulators of every aspect of gut function. Many GPCRs are internalised upon activation, and this represents one of the mechanisms through which G protein-signalling is terminated. The latency between the endocytosis of GPCRs and their recycling and resensitization is a major determinant of the cell's ability to respond to subsequent exposure to agonists.
MeSH term(s)	Animals ; Enteric Nervous System/metabolism ; GTP-Binding Proteins/metabolism ; Protein Transport ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, G-Protein-Coupled ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2016-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	410187-X
ISSN	0065-2598
ISSN	0065-2598
DOI	10.1007/978-3-319-27592-5_14
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Zs.A 3192: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: G protein-coupled receptor trafficking and signaling: new insights into the enteric nervous system.

Carbone, Simona E / Veldhuis, Nicholas A / Gondin, Arisbel B / Poole, Daniel P

American journal of physiology. Gastrointestinal and liver physiology

2019 Volume 316, Issue 4, Page(s) G446–G452

Abstract: G protein-coupled receptors (GPCRs) are essential for the neurogenic control of gastrointestinal (GI) function and are important and emerging therapeutic targets in the gut. Detailed knowledge of both the distribution and functional expression of GPCRs ... ...

Abstract	G protein-coupled receptors (GPCRs) are essential for the neurogenic control of gastrointestinal (GI) function and are important and emerging therapeutic targets in the gut. Detailed knowledge of both the distribution and functional expression of GPCRs in the enteric nervous system (ENS) is critical toward advancing our understanding of how these receptors contribute to GI function during physiological and pathophysiological states. Equally important, but less well defined, is the complex relationship between receptor expression, ligand binding, signaling, and trafficking within enteric neurons. Neuronal GPCRs are internalized following exposure to agonists and under pathological conditions, such as intestinal inflammation. However, the relationship between the intracellular distribution of GPCRs and their signaling outputs in this setting remains a "black box". This review will briefly summarize current knowledge of agonist-evoked GPCR trafficking and location-specific signaling in the ENS and identifies key areas where future research could be focused. Greater understanding of the cellular and molecular mechanisms involved in regulating GPCR signaling in the ENS will provide new insights into GI function and may open novel avenues for therapeutic targeting of GPCRs for the treatment of digestive disorders.
MeSH term(s)	Animals ; Drug Discovery ; Enteric Nervous System/physiology ; Enterocytes/physiology ; Humans ; Protein Transport/drug effects ; Protein Transport/physiology ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction
Chemical Substances	Receptors, G-Protein-Coupled
Language	English
Publishing date	2019-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00406.2018
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Article ; Online: Role of Nonneuronal TRPV4 Signaling in Inflammatory Processes.

Rajasekhar, Pradeep / Poole, Daniel P / Veldhuis, Nicholas A

Advances in pharmacology (San Diego, Calif.)

2017 Volume 79, Page(s) 117–139

Abstract: Transient receptor potential (TRP) ion channels are important signaling components in nociceptive and inflammatory pathways. This is attributed to their ability to function as polymodal sensors of environmental stimuli (chemical and mechanical) and as ... ...

Abstract	Transient receptor potential (TRP) ion channels are important signaling components in nociceptive and inflammatory pathways. This is attributed to their ability to function as polymodal sensors of environmental stimuli (chemical and mechanical) and as effector molecules in receptor signaling pathways. TRP vanilloid 4 (TRPV4) is a nonselective cation channel that is activated by multiple endogenous stimuli including shear stress, membrane stretch, and arachidonic acid metabolites. TRPV4 contributes to many important physiological processes and dysregulation of its activity is associated with chronic conditions of metabolism, inflammation, peripheral neuropathies, musculoskeletal development, and cardiovascular regulation. Mechanosensory and receptor- or lipid-mediated signaling functions of TRPV4 have historically been attributed to central and peripheral neurons. However, with the development of potent and selective pharmacological tools, transgenic mice and improved molecular and imaging techniques, many new roles for TRPV4 have been revealed in nonneuronal cells. In this chapter, we discuss these recent findings and highlight the need for greater characterization of TRPV4-mediated signaling in nonneuronal cell types that are either directly associated with neurons or indirectly control their excitability through release of sensitizing cellular factors. We address the integral role of these cells in sensory and inflammatory processes as well as their importance when considering undesirable on-target effects that may be caused by systemic delivery of TRPV4-selective pharmaceutical agents for treatment of chronic diseases. In future, this will drive a need for targeted drug delivery strategies to regulate such a diverse and promiscuous protein.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1557-8925
ISSN (online)	1557-8925
DOI	10.1016/bs.apha.2017.03.002
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Article ; Online: Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels.

Keely, Stephen J / Urso, Andreacarola / Ilyaskin, Alexandr V / Korbmacher, Christoph / Bunnett, Nigel W / Poole, Daniel P / Carbone, Simona E

American journal of physiology. Gastrointestinal and liver physiology

2021 Volume 322, Issue 2, Page(s) G201–G222

Abstract: Bile acids (BAs) are known to be important regulators of intestinal motility and epithelial fluid and electrolyte transport. Over the past two decades, significant advances in identifying and characterizing the receptors, transporters, and ion channels ... ...

Abstract	Bile acids (BAs) are known to be important regulators of intestinal motility and epithelial fluid and electrolyte transport. Over the past two decades, significant advances in identifying and characterizing the receptors, transporters, and ion channels targeted by BAs have led to exciting new insights into the molecular mechanisms involved in these processes. Our appreciation of BAs, their receptors, and BA-modulated ion channels as potential targets for the development of new approaches to treat intestinal motility and transport disorders is increasing. In the current review, we aim to summarize recent advances in our knowledge of the different BA receptors and BA-modulated ion channels present in the gastrointestinal system. We discuss how they regulate motility and epithelial transport, their roles in pathogenesis, and their therapeutic potential in a range of gastrointestinal diseases.
MeSH term(s)	Bile Acids and Salts/metabolism ; Gastrointestinal Tract/drug effects ; Humans ; Ion Channels/agonists ; Ion Channels/drug effects ; Liver/drug effects ; Receptors, Calcitriol/drug effects ; Sodium Channels/drug effects
Chemical Substances	Bile Acids and Salts ; Ion Channels ; Receptors, Calcitriol ; Sodium Channels
Language	English
Publishing date	2021-11-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00125.2021
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