Evidence map›Paper›PMID 26330151›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2015

Transient receptor potential vanilloid 4 inhibits mouse colonic motility by activating NO-dependent enteric neurotransmission.

J Fichna, D P Poole, N Veldhuis, S J MacEachern, D Saur, P K Zakrzewski, A I Cygankiewicz, A Mokrowiecka, E Małecka-Panas, W M Krajewska and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Role of TRPV4 in the Diagnosis and Treatment ofBioMed research international · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 8 institutions in 6 countries.

J FichnaSnyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada.
D P PooleMonash Institute of Pharmaceutical Sciences, Parkville, Victoria, Australia.
N VeldhuisMonash Institute of Pharmaceutical Sciences, Parkville, Victoria, Australia.
S J MacEachernDepartment of Physiology & Pharmacology, University of Calgary, Calgary, AB, Canada.
D SaurII Medizinische Klinik, Technische Universität München, Munich, Germany.
P K ZakrzewskiDepartment of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
A I CygankiewiczDepartment of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
A MokrowieckaDepartment of Digestive Tract Diseases, Faculty of Medicine, Medical University of Lodz, Lodz, Poland.
E Małecka-PanasDepartment of Digestive Tract Diseases, Faculty of Medicine, Medical University of Lodz, Lodz, Poland.
W M KrajewskaDepartment of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
W LiedtkeCenter for Translational Neuroscience, Duke University, Durham, NC, USA.
M S SteinhoffDepartment of Dermatology and Surgery, University of California San Francisco, San Francisco, CA, USA.
J-P TimmermansLaboratory of Cell Biology and Histology, Department of Veterinary Sciences, University of Antwerp, Antwerp, Belgium.
N W BunnettMonash Institute of Pharmaceutical Sciences, Parkville, Victoria, Australia.
K A SharkeySnyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada.
M A StorrSnyder Institute for Chronic Diseases, University of Calgary, Calgary, AB, Canada. martin.storr@med.uni-muenchen.de.
University of Calgary · CAUniversity of Łódź · PLMedical University of Lodz · PLThe University of Melbourne · AUDuke University · USTechnical University of Munich · DEUniversity of Antwerp · BEUniversity of California, San Francisco · US

Funding

PROTEINASE-ACTIVATED RECEPTORS/PERIPHERAL NERVOUS SYSTEMR01DK057840 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUNNETT, NIGEL W · 2000 to 2010
$2.2M
Canadian Institutes of Health ResearchNIDDK NIH HHS DK57840
6 · The paper itself

Abstract

unlabelledRecent studies implicate TRPV4 receptors in visceral pain signaling and intestinal inflammation. Our aim was to evaluate the role of TRPV4 in the control of gastrointestinal (GI) motility and to establish the underlying mechanisms. We used immunohistochemistry and PCR to study TRPV4 expression in the GI tract. The effect of TRPV4 activation on GI motility was characterized using in vitro and in vivo motility assays. Calcium and nitric oxide (NO) imaging were performed to study the intracellular signaling pathways. Finally, TRPV4 expression was examined in the colon of healthy human subjects. We demonstrated that TRPV4 can be found on myenteric neurons of the colon and is co-localized with NO synthase (NOS-1). In vitro, the TRPV4 agonist GSK1016790A reduced colonic contractility and increased inhibitory neurotransmission. In vivo, TRPV4 activation slowed GI motility and reduced stool production in mouse models mimicking pathophysiological conditions. We also showed that TRPV4 activation inhibited GI motility by reducing NO-dependent Ca(2+) release from enteric neurons. In conclusion, TRPV4 is involved in the regulation of GI motility in health and disease. KEY MESSAGES: • Recent studies implicate TRPV4 in pain signaling and intestinal inflammation. • Our aim was to characterize the role of TRPV4 in the control of GI motility. • We found that TRPV4 activation reduced colonic contractility. • Our studies also showed altered TRPV4 mRNA expression in IBS-C patients. • TRPV4 may be a novel pharmacological target in functional GI diseases.

Indexed as

AdultAgedAged, 80 and overAnimalsCase-Control StudiesColonDisease Models, AnimalFemaleGastrointestinal MotilityGene ExpressionGuanylate CyclaseHumansIrritable Bowel SyndromeLeucineMaleMiceGuanylate CyclaseLeucineN-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamideNitric OxideNitric Oxide SynthaseSulfonamidesTRPV4 protein, humanTRPV Cation ChannelsIrritable bowel syndromeMyenteric plexusNitric oxide synthase type 1

Identifiers

PMID26330151
OpenAlexW1211522970

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.