Evidence map›Paper›PMID 22410640›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2012

The involvement of oxidants and NF-κB in cytokine-induced MMP-9 synthesis by bone marrow-derived osteoprogenitor cells.

Dror Ben-David, Erella Livne, Abraham Z Reznick

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  5. TRAF6 is required for BLyS-mediated NF-κB signaling in multiple myeloma cells.Medical oncology (Northwood, London, England) · 2015
    Article
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  8. Effect of TRAF6 on the biological behavior of human lung adenocarcinoma cell.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  9. Article
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

3 authors at 1 institution in 1 country.

Dror Ben-DavidDepartment of Anatomy and Cell Biology, Faculty of Medicine, Technion, P.O. Box 9649, 31096 Haifa, Israel.
Erella Livne
Abraham Z Reznick
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designThe activity of immune cells affects the balance between bone mineralization and resorption carried out by the opposing actions of osteoblasts and osteoclasts, respectively. This study was aimed at determining the possible interaction between inflammatory conditions and collagen type I degrading MMP (mainly MMP-2 and MMP-9) synthesis and secretion in rat osteoprogenitors. MATERIALS AND

methodsThe study was performed using primary rat bone marrow-derived osteoprogenitors during their advanced osteogenesis. Biochemical, immunohistochemical, and molecular biology techniques were used to investigate the influence of pro-inflammatory cytokines on MMP-2 and MMP-9 synthesis and secretion in osteoprogenitors.

resultsResults indicated that both synthesis and secretion of MMPs (MMP-1, -2, -8, -9, and -13) were significantly induced after pro-inflammatory cytokine treatments, except MMP-2, whose levels remained unchanged. NF-κB (nuclear factor kappa-light chain enhancer of activated B cells) inhibition assays showed that induced MMP-9 secretion by inflammatory cytokines was mediated by activation of NF-κB via the classical pathway and that oxidants play a significant role in this signal transduction pathway. In contrast, no such effect was observed for synthesis of MMP-2.

conclusionsThese results indicate the possibility that inflammatory processes may trigger osteoblasts to absorb bone by secreting elevated levels of MMPs capable of degrading collagen type I, especially MMP-9 which is upregulated due to increased NF-κB transcription activity.

Indexed as

AcetylcysteineAnimalsAntioxidantsBone Marrow CellsButylated HydroxytolueneCells, CulturedCollagen Type II-kappa B ProteinsInterleukin-1alphaMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mesenchymal Stem CellsNF-kappa BNF-KappaB Inhibitor alphaRatsRats, Sprague-DawleyAcetylcysteineAntioxidantsButylated HydroxytolueneCollagen Type II-kappa B ProteinsInterleukin-1alphaMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, ratMmp9 protein, ratNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID22410640
OpenAlexW2024091112

What OpenQuestion holds

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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.