Evidence map›Paper›PMID 19248089›Full record

ArticleArthritis and rheumatism2009

Interleukin-1beta and tumor necrosis factor alpha inhibit chondrogenesis by human mesenchymal stem cells through NF-kappaB-dependent pathways.

N Wehling, G D Palmer, C Pilapil, F Liu, J W Wells, P E Müller, C H Evans, R M Porter

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

141 citing papers in PubMed, 2 syntheses or guidelines pooled it, 233 citations in OpenAlex.

  1. TNFα-Related Chondrocyte Inflammation Models: A Systematic Review.International journal of molecular sciences · 2024
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  18. Bioengineering (Basel, Switzerland) · 2025
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81 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

N WehlingCampus Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
G D Palmer
C Pilapil
F Liu
J W Wells
P E Müller
C H Evans
R M Porter
Harvard University · USCenter for Orthopaedics · USLudwig-Maximilians-Universität München · DE

Funding

Gene-activated Bone Marrow Plugs for Cartilage RepairF32EB005566 · NIBIB · BRIGHAM AND WOMEN'S HOSPITAL · PI PORTER, RYAN MICHAEL · 2006 to 2007
$90k
NIBIB NIH HHS F32 EB005566NIBIB NIH HHS F32-EB-005566
6 · The paper itself

Abstract

objectiveThe differentiation of mesenchymal stem cells (MSCs) into chondrocytes provides an attractive basis for the repair and regeneration of articular cartilage. Under clinical conditions, chondrogenesis will often need to occur in the presence of mediators of inflammation produced in response to injury or disease. The purpose of this study was to examine the effects of 2 important inflammatory cytokines, interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha), on the chondrogenic behavior of human MSCs.

methodsAggregate cultures of MSCs recovered from the femoral intermedullary canal were used. Chondrogenesis was assessed by the expression of relevant transcripts by quantitative reverse transcription-polymerase chain reaction analysis and examination of aggregates by histologic and immunohistochemical analyses. The possible involvement of NF-kappaB in mediating the effects of IL-1beta was examined by delivering a luciferase reporter construct and a dominant-negative inhibitor of NF-kappaB (suppressor-repressor form of IkappaB [srIkappaB]) with adenovirus vectors.

resultsBoth IL-1beta and TNFalpha inhibited chondrogenesis in a dose-dependent manner. This was associated with a marked activation of NF-kappaB. Delivery of srIkappaB abrogated the activation of NF-kappaB and rescued the chondrogenic response. Although expression of type X collagen followed this pattern, other markers of hypertrophic differentiation responded differently. Matrix metalloproteinase 13 was induced by IL-1beta in a NF-kappaB-dependent manner. Alkaline phosphatase activity, in contrast, was inhibited by IL-1beta regardless of srIkappaB delivery.

conclusionCell-based repair of lesions in articular cartilage will be compromised in inflamed joints. Strategies for enabling repair under these conditions include the use of specific antagonists of individual pyrogens, such as IL-1beta and TNFalpha, or the targeting of important intracellular mediators, such as NF-kappaB.

Indexed as

AgedCell DifferentiationCells, CulturedChondrogenesisCollagen Type XFemaleHumansInterleukin-1betaMaleMatrix Metalloproteinase 13Mesenchymal Stem CellsNF-kappa BSignal TransductionTransforming Growth Factor beta1Tumor Necrosis Factor-alphaCollagen Type XInterleukin-1betaMatrix Metalloproteinase 13NF-kappa BTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID19248089
PMCPMC2688727
OpenAlexW1990205367

What OpenQuestion holds

Textmetadata
LicenceTDM
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.