Evidence map›Paper›PMID 33568699›Full record

ArticleScientific reports2021

TRPV1 feed-forward sensitisation depends on COX2 upregulation in primary sensory neurons.

Tianci Li, Gaoge Wang, Vivian Chin Chin Hui, Daniel Saad, Joao de Sousa Valente, Paolo La Montanara, Istvan Nagy

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Tianci LiNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK.
Gaoge WangNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK.
Vivian Chin Chin HuiNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK.
Daniel SaadNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK.
Joao de Sousa ValenteSection of Vascular Biology and Inflammation Section, School of Cardiovascular Medicine and Sciences, BHF Centre of Research Excellence, King's College London, London, UK.
Paolo La MontanaraNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK.
Istvan NagyNociception Group, Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Chelsea and Westminster Hospital, Imperial College London, 369 Fulham Road, London, SW10 9NH, UK. i.nagy@imperial.ac.uk.
Imperial College London · GBChelsea and Westminster Hospital · GBKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased activity and excitability (sensitisation) of a series of molecules including the transient receptor potential ion channel, vanilloid subfamily, member 1 (TRPV1) in pain-sensing (nociceptive) primary sensory neurons are pivotal for developing pathological pain experiences in tissue injuries. TRPV1 sensitisation is induced and maintained by two major mechanisms; post-translational and transcriptional changes in TRPV1 induced by inflammatory mediators produced and accumulated in injured tissues, and TRPV1 activation-induced feed-forward signalling. The latter mechanism includes synthesis of TRPV1 agonists within minutes, and upregulation of various receptors functionally linked to TRPV1 within a few hours, in nociceptive primary sensory neurons. Here, we report that a novel mechanism, which contributes to TRPV1 activation-induced TRPV1-sensitisation within ~ 30 min in at least ~ 30% of TRPV1-expressing cultured murine primary sensory neurons, is mediated through upregulation in cyclooxygenase 2 (COX2) expression and increased synthesis of a series of COX2 products. These findings highlight the importance of feed-forward signalling in sensitisation, and the value of inhibiting COX2 activity to control pain, in nociceptive primary sensory neurons in tissue injuries.

Indexed as

AnimalsCapsaicinCyclooxygenase 2Ganglia, SpinalInflammation MediatorsMiceNeuronsPainTransient Receptor Potential ChannelsTRPV Cation ChannelsUp-RegulationCapsaicinCyclooxygenase 2Inflammation MediatorsTransient Receptor Potential ChannelsTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID33568699
PMCPMC7876133
OpenAlexW3129181052

What OpenQuestion holds

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Registered trials

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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.