Evidence map›Paper›PMID 26521733›Full record

ArticleOsteoarthritis and cartilage2015

Deficiency of hyaluronan synthase 1 (Has1) results in chronic joint inflammation and widespread intra-articular fibrosis in a murine model of knee joint cartilage damage.

D D Chan, W F Xiao, J Li, C A de la Motte, J D Sandy, A Plaas

Abstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  17. The gut microbiota may be a novel pathogenic mechanism in loosening of orthopedic implants in rats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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 3 institutions in 2 countries.

D D ChanDivision of Rheumatology, Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA. Electronic address: deva_chan@rush.edu.
W F XiaoDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: wenfeng_xiao@163.com.
J LiDivision of Rheumatology, Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA. Electronic address: jun_li@rush.edu.
C A de la MotteDepartment of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: delamoc@ccf.org.
J D SandyDepartment of Biochemistry, Rush University Medical Center, Chicago, IL, USA; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA. Electronic address: jsandy44@gmail.com.
A PlaasDivision of Rheumatology, Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA; Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA. Electronic address: anna_plaas@rush.edu.
Rush University Medical Center · USCentral South University · CNCleveland Clinic Lerner College of Medicine · US

Funding

Cartilage Degeneration and Repair By ADAMTSs and Hyaluronan Binding ProteinsR01AR057066 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI PLAAS, ANNA H. · 2011 to 2015
$1.7M
NIAMS NIH HHS R01 AR057066NIAMS NIH HHS R01-AR057066
6 · The paper itself

Abstract

objectiveArticular cartilage defects commonly result from traumatic injury and predispose to degenerative joint diseases. To test the hypothesis that aberrant healing responses and chronic inflammation lead to osteoarthritis (OA), we examined spatiotemporal changes in joint tissues after cartilage injury in murine knees. Since intra-articular injection of hyaluronan (HA) can attenuate injury-induced osteoarthritis in wild-type (WT) mice, we investigated a role for HA in the response to cartilage injury in mice lacking HA synthase 1 (Has1(-/-)).

designFemoral groove cartilage of WT and Has1(-/-) mice was debrided to generate a non-bleeding wound. Macroscopic imaging, histology, and gene expression were used to evaluate naïve, sham-operated, and injured joints.

resultsAcute responses (1-2 weeks) in injured joints from WT mice included synovial hyperplasia with HA deposition and joint-wide increases in expression of genes associated with inflammation, fibrosis, and extracellular matrix (ECM) production. By 4 weeks, some resurfacing of damaged cartilage occurred, and early cell responses were normalized. Cartilage damage in Has1(-/-) mice also induced early responses; however, at 4 weeks, inflammation and fibrosis genes remained elevated with widespread cartilage degeneration and fibrotic scarring in the synovium and joint capsule.

conclusionsWe conclude that the ineffective repair of injured cartilage in Has1(-/-) joints can be at least partly explained by the markedly enhanced expression of particular genes in pathways linked to ECM turnover, IL-17/IL-6 cytokine signaling, and apoptosis. Notably, Has1 ablation does not alter gross HA content in the ECM, suggesting that HAS1 has a unique function in the metabolism of inflammatory HA matrices.

Indexed as

Gene Expression RegulationAnimalsCartilage, ArticularChronic DiseaseDisease Models, AnimalFibrosisGlucuronosyltransferaseHyaluronan SynthasesInflammationKnee JointMaleMiceMice, Inbred C57BLOsteoarthritis, KneePolymerase Chain ReactionRNAGlucuronosyltransferaseHyaluronan SynthasesRNACartilageFibrotic scarHyaluronan synthasesInflammationInjurySynovium

Identifiers

PMID26521733
PMCPMC4630789
OpenAlexW1923514176

What OpenQuestion holds

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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.