Evidence map›Paper›PMID 19805379›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Chromatin protein HMGB2 regulates articular cartilage surface maintenance via beta-catenin pathway.

Noboru Taniguchi, Beatriz Caramés, Yasuhiko Kawakami, Brad A Amendt, Setsuro Komiya, Martin Lotz

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-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

38 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  6. Article
  7. Structure and Functions of HMGB2 Protein.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
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  11. Article
  12. Review
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  15. Review
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  19. Article
  20. Mesenchymal Stem Cells for Osteochondral Tissue Engineering.Methods in molecular biology (Clifton, N.J.) · 2016
    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

6 authors at 4 institutions in 2 countries.

Noboru TaniguchiDepartment of Arthritis Research, The Scripps Research Institute, La Jolla, CA 92037, USA.
Beatriz Caramés
Yasuhiko Kawakami
Brad A Amendt
Setsuro Komiya
Martin Lotz
Scripps Research Institute · USKagoshima University · JPTexas A&M University System · USUniversity of Minnesota · US

Funding

TISSUE ACQUISITION, MORPHOLOGY, AND CELL CULTUREP01AG007996 · NIA · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SAH, ROBERT L · 1989 to 2016
$26.0M
CHONDROCYTE SUBPOPULATIONS IN AGING AND OSTEOARTHRITISR01AG033409 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI LOTZ, MARTIN K · 2008 to 2008
$544k
NIA NIH HHS AG 007996NIA NIH HHS AG 033409NIA NIH HHS P01 AG007996NIA NIH HHS R01 AG033409
6 · The paper itself

Abstract

The superficial zone (SZ) of articular cartilage is critical in maintaining tissue function and homeostasis and represents the site of the earliest changes in osteoarthritis. Mechanisms that regulate the unique phenotype of SZ chondrocytes and maintain SZ integrity are unknown. We recently demonstrated that expression of the chromatin protein high mobility group box (HMGB) protein 2 is restricted to the SZ in articular cartilage suggesting a transcriptional regulation involving HMGB2 in SZ. Here, we show that an interaction between HMGB2 and the Wnt/beta-catenin pathway regulates the maintenance of the SZ. We found that the Wnt/beta-catenin pathway is active specifically in the SZ in normal mouse knee joints and colocalizes with HMGB2. Both Wnt signaling and HMGB2 expression decrease with aging in mouse joints. Our molecular studies show that HMGB2 enhances the binding of Lef-1 to its target sequence and potentiates transcriptional activation of the Lef-1-beta-catenin complex. The HMG domain within HMGB2 is crucial for interaction with Lef-1, suggesting that both HMGB2 and HMGB1 may be involved in this function. Furthermore, conditional deletion of beta-catenin in cultured mouse chondrocytes induced apoptosis. These findings define a pathway where protein interactions of HMGB2 and Lef-1 enhance Wnt signaling and promote SZ chondrocyte survival. Loss of the HMGB2-Wnt signaling interaction is a new mechanism in aging-related cartilage pathology.

Indexed as

Signal TransductionAnimalsApoptosisbeta CateninBinding SitesCartilage, ArticularHMGB2 ProteinLymphoid Enhancer-Binding Factor 1MiceMice, Inbred StrainsWnt Proteinsbeta CateninHMGB2 ProteinLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Wnt Proteins

Identifiers

PMID19805379
PMCPMC2757822
OpenAlexW2011516741

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.