Evidence map›Paper›PMID 12670873›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2003

A central role for the nuclear factor-kappaB pathway in anti-inflammatory and proinflammatory actions of mechanical strain.

Sudha Agarwal, Ping Long, Al Seyedain, Nicholas Piesco, Anu Shree, Robert Gassner

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 82 citations in OpenAlex.

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  11. Conditional Activation of NF-κB Inducing Kinase (NIK) in the Osteolineage Enhances Both Basal and Loading-Induced Bone Formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
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  20. Mechanosignaling in bone health, trauma and inflammation.Antioxidants & redox signaling · 2014
    Review
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

6 authors at 2 institutions in 1 country.

Sudha AgarwalMcGowen Institute of Regenerative, 589 Salk Hall, University of Pittsburgh, 3501 Terrace St., Pittsburgh, Pennsylvania 15261-1964, USA. sagar@pitt.edu
Ping Long
Al Seyedain
Nicholas Piesco
Anu Shree
Robert Gassner
McGowan Institute for Regenerative Medicine · USUniversity of Pittsburgh · US

Funding

Inflammation of TMJDs: Role of Biomechanical SignalsR01DE015399 · NIDCR · OHIO STATE UNIVERSITY · PI AGARWAL, SUDHA · 2003 to 2006
$1.4M
STRESS-INDUCED ANTI-INFLAMMATORY SIGNALS IN CHONDROCYTESR01AT000646 · NCCIH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2000 to 2004
$1.1M
NCCIH NIH HHS R01 AT000646NIDCR NIH HHS R01 DE015399
6 · The paper itself

Abstract

Mechanical signals play an integral role in bone homeostasis. These signals are observed at the interface of bone and teeth, where osteoblast-like periodontal ligament (PDL) cells constantly take part in bone formation and resorption in response to applied mechanical forces. Earlier, we reported that signals generated by tensile strain of low magnitude (TENS-L) are antiinflammatory, whereas tensile strain of high magnitude (TENS-H) is proinflammatory and catabolic. In this study, we examined the mechanisms of intracellular actions of the antiinflammatory and proinflammatory signals generated by TENS of various magnitudes. We show that both low and high magnitudes of mechanical strain exploit nuclear factor (NF)-kappaB as a common pathway for transcriptional inhibition/activation of proinflammatory genes and catabolic processes. TENS-L is a potent inhibitor of interleukin (IL)-1 beta-induced I-kappaBbeta degradation and prevents dissociation of NF-kB from cytoplasmic complexes and thus its nuclear translocation. This leads to sustained suppression of IL-1beta-induced NF-kappaB transcriptional regulation of proinflammatory genes. In contrast, TENS-H is a proinflammatory signal that induces I-kappaBbeta degradation, nuclear translocation of NF-kappaB, and transcriptional activation of proinflammatory genes. These findings are the first to describe the largely unknown intracellular mechanism of action of applied tensile forces in osteoblast-like cells and have critical implications in bone remodeling.

Indexed as

Binding SitesBiological TransportCell NucleusCells, CulturedCyclooxygenase 2DinoprostoneGene Expression Regulation, EnzymologicHumansInterleukin-1IsoenzymesMembrane ProteinsNF-kappa BPeriodontal LigamentProstaglandin-Endoperoxide SynthasesRNA, MessengerSignal TransductionCyclooxygenase 2DinoprostoneInterleukin-1IsoenzymesMembrane ProteinsNF-kappa BProstaglandin-Endoperoxide SynthasesPTGS2 protein, humanRNA, Messenger

Identifiers

PMID12670873
PMCPMC4955537
OpenAlexW2116421111

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.