Evidence map›Paper›PMID 23313877›Full record

ArticleGene2013

Bovine lactoferricin induces TIMP-3 via the ERK1/2-Sp1 axis in human articular chondrocytes.

Dongyao Yan, Di Chen, John R Hawse, Andre J van Wijnen, Hee-Jeong Im

Open access · greenAbstract readComparative Study
In one paragraph

Article in Gene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. TIMP-3 as a therapeutic target for cancer.Therapeutic advances in medical oncology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

5 authors at 3 institutions in 1 country.

Dongyao YanDepartment of Biochemistry, Section of Rheumatology, Rush University Medical Center, Chicago, IL 60612, USA.
Di Chen
John R Hawse
Andre J van Wijnen
Hee-Jeong Im
Mayo Clinic · USRush University Medical Center · USUniversity of Illinois Chicago · US

Funding

Molecular Control of Bone FormationR01AR049069 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WESTENDORF, JENNIFER J · 2003 to 2021
$5.8M
Role of a TGF-? Regulated Gene in Human and Mouse Osteoblasts and SkeletonR01DE014036 · NIDCR · MAYO CLINIC ROCHESTER · PI HAWSE, JOHN R., SUBRAMANIAM, MALAYANNAN · 2001 to 2016
$4.7M
The Mechanism through which TGF-Beta Maintains Chondrocytes in Proliferating StagR01AR054465 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2007 to 2018
$2.7M
Pain Mechanisms of Knee Joint OsteoarthritisR01AR062136 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI CHEN, DI · 2012 to 2016
$1.7M
Beta-Catenin Signaling and Pathogenesis of OsteoarthritisR01AR055915 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2009 to 2013
$1.7M
Pathological Role of bFGF in Human Adult Articular CartilageR01AR053220 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI SAMPEN, HEE-JEONG IM · 2006 to 2010
$1.6M
Role of aTGF-beta Regulated Gene in human and mouse osteoblasts and skeletonR56DE014036 · NIDCR · MAYO CLINIC ROCHESTER · PI SPELSBERG, THOMAS C · 2007 to 2007
$352k
OSTEOARTHRITIS AND KNEE JOINT PAINI01BX002647 · VA · JESSE BROWN VA MEDICAL CENTER · PI SAMPEN, HEE-JEONG IM · 2015 to 2023
–
BLRD VA I01 BX002647NIAMS NIH HHS AR053220NIAMS NIH HHS AR062136NIAMS NIH HHS R01 AR049069NIAMS NIH HHS R01 AR053220NIAMS NIH HHS R01 AR054465NIAMS NIH HHS R01 AR055915NIAMS NIH HHS R01 AR062136NIDCR NIH HHS DE014036NIDCR NIH HHS R01 DE014036NIDCR NIH HHS R56 DE014036
6 · The paper itself

Abstract

Bovine lactoferricin (LfcinB) is a heparan sulfate-binding peptide with multiple bioactivities. In human articular cartilage, LfcinB antagonizes interleukin-1 β (IL-1β) and fibroblast growth factor 2 (FGF-2) in proteoglycan metabolism, catabolic protease expression, and induction of pro-inflammatory mediators. LfcinB specifically activates ERK1/2, p38 and Akt, but whether these signaling pathways control the expression of LfcinB target genes remained unknown. In this report, we characterized a novel aspect of LfcinB-mediated genetic response in human articular chondrocytes, tissue inhibitor of metalloproteinase 3 (TIMP-3) induction. Inhibition of individual signaling pathways revealed that ERK1/2 functions as the major pathway in TIMP-3 expression, whereas Akt plays a minor role. Further investigation identified Sp1 as a critical transcriptional activator in TIMP-3 regulation, and Sp1 activity is modulated by ERK1/2, not Akt. Comparative quantification indicates that significant downregulation of TIMP-3 occurs in OA chondrocytes, suggesting a beneficial role of LfcinB in OA pathogenesis. Our results collectively provide new insights into the mechanism of action of LfcinB, and support the candidacy of LfcinB as a chondroprotective agent.

Indexed as

AdultAgedAnimalsAnti-Bacterial AgentsBlotting, WesternCartilage, ArticularCase-Control StudiesCattleCells, CulturedChondrocytesElectrophoretic Mobility Shift AssayHumansImmunoenzyme TechniquesLactoferrinMiddle AgedMitogen-Activated Protein Kinase 1Anti-Bacterial Agentslactoferricin BLactoferrinMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3RNA, MessengerSp1 Transcription FactorTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3

Identifiers

PMID23313877
PMCPMC3573330
OpenAlexW1998583251

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.