Evidence map›Paper›PMID 19695100›Full record

ArticleMolecular pain2009

Tumor necrosis factor-alpha (TNF-alpha) enhances functional thermal and chemical responses of TRP cation channels in human synoviocytes.

Mikhail Y Kochukov, Terry A McNearney, Huaizhi Yin, Liping Zhang, Fei Ma, Larissa Ponomareva, Sarah Abshire, Karin N Westlund

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

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  12. TRPV4 and TRPM8 as putative targets for chronic low back pain alleviation.Pflugers Archiv : European journal of physiology · 2021
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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

8 authors at 2 institutions in 1 country.

Mikhail Y KochukovDepartment of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA. mykochuk@utmb.edu
Terry A McNearney
Huaizhi Yin
Liping Zhang
Fei Ma
Larissa Ponomareva
Sarah Abshire
Karin N Westlund
Albert B. Chandler Hospital · USThe University of Texas Medical Branch at Galveston · US

Funding

VISCERAL PAINP01NS011255 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI NEUGEBAUER, VOLKER · 1985 to 2012
$13.6M
Glutamate Induced Molecular Events Contributing to Chro*R21AR048371 · NIAMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WESTLUND-HIGH, KARIN N · 2001 to 2002
$149k
CENTRAL CONTROL OF ARTHRITIS AND ARTHRITIC PAINR01NS032778 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WESTLUND-HIGH, KARIN N · 1995 to 1998
–
NINDS NIH HHS NS11255NINDS NIH HHS NS 32778
6 · The paper itself

Abstract

backgroundWe have shown functional expression of several TRP channels on human synovial cells, proposing significance in known calcium dependent proliferative and secretory responses in joint inflammation. The present study further characterizes synoviocyte TRP expression and activation responses to thermal and osmotic stimuli after pre-treatment with proinflammatory mediator tumor necrosis factor alpha (TNF-alpha, EC50 1.3221 x 10(-10) g/L).

resultsFluorescent imaging of Fura-2 loaded human SW982 synoviocytes reveals immediate and delayed cytosolic calcium oscillations elicited by (1) TRPV1 agonists capsaicin and resiniferatoxin (20-40% of cells), (2) moderate and noxious temperature change, and (3) osmotic stress TRPV4 activation (11.5% of cells). TNF-alpha pre-treatment (1 ng/ml, 8-16 hr) significantly increases (doubles) capsaicin responsive cell numbers and [Ca2+]i spike frequency, as well as enhances average amplitude of temperature induced [Ca2+]i responses. With TNF-alpha pre-treatment for 8, 12, and 16 hr, activation with 36 or 45 degree bath solution induces bimodal [Ca2+]i increase (temperature controlled chamber). Initial temperature induced rapid transient spikes and subsequent slower rise reflect TRPV1 and TRPV4 channel activation, respectively. Only after prolonged TNF-alpha exposure (12 and 16 hr) is recruitment of synoviocytes observed with sensitized TRPV4 responses to hypoosmolarity (3-4 fold increase). TNF-alpha increases TRPV1 (8 hr peak) and TRPV4 (12 hr peak) immunostaining, mRNA and protein expression, with a TRPV1 shift to membrane fractions.

conclusionTNF-alpha provides differentially enhanced synoviocyte TRPV1 and TRPV4 expression and [Ca2+]i response dependent on the TRP stimulus and time after exposure. Augmented relevance of TRPV1 and TRPV4 as inflammatory conditions persist would provide calcium mediated cell signaling required for pathophysiological responses of synoviocytes in inflammatory pain states.

Indexed as

CapsaicinCell LineDiterpenesGene ExpressionHumansOsmotic PressureSensory System AgentsSynovial MembraneTemperatureTransient Receptor Potential ChannelsTRPV Cation ChannelsTumor Necrosis Factor-alphaCapsaicinDiterpenesresiniferatoxinSensory System AgentsTransient Receptor Potential ChannelsTRPV Cation ChannelsTumor Necrosis Factor-alpha

Identifiers

PMID19695100
PMCPMC3152771
OpenAlexW2105523906

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.