Evidence map›Paper›PMID 31253842›Full record

ArticleNature communications2019

The microRNAs miR-204 and miR-211 maintain joint homeostasis and protect against osteoarthritis progression.

Jian Huang, Lan Zhao, Yunshan Fan, Lifan Liao, Peter X Ma, Guozhi Xiao, Di Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
17.1field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 168 citations in OpenAlex.

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47 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

7 authors at 2 institutions in 1 country.

Jian HuangDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA.ORCID http://orcid.org/0000-0002-6676-5159
Lan ZhaoDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA.ORCID http://orcid.org/0000-0003-0865-2006
Yunshan FanDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA.
Lifan LiaoDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA.
Peter X MaDepartment of Biologic and Materials Science, University of Michigan, Ann Arbor, MI, 48109, USA.ORCID http://orcid.org/0000-0002-0191-9487
Guozhi XiaoDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA.
Di ChenDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, 60612, USA. di_chen@rush.edu.
Rush University Medical Center · USUniversity of Michigan · US

Funding

The Mechanism through which TGF-Beta Maintains Chondrocytes in Proliferating StagR01AR054465 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2007 to 2018
$2.7M
The Role of MicroRNA in Osteoarthritis: Alzheimer's Administrative SupplementR01AR070222 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI HUANG, JIAN, ZHAO, LAN · 2017 to 2022
$2.1M
National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund) 81630066NIAMS NIH HHS R01 AR054465NIAMS NIH HHS R01 AR070222U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R01AR054465U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R01AR070222
6 · The paper itself

Abstract

Osteoarthritis (OA) is a common, painful disease. Currently OA is incurable, and its etiology largely unknown, partly due to limited understanding of OA as a whole-joint disease. Here we report that two homologous microRNAs, miR-204 and miR-211, maintain joint homeostasis to suppress OA pathogenesis. Specific knockout of miR-204/-211 in mesenchymal progenitor cells (MPCs) results in Runx2 accumulation in multi-type joint cells, causing whole-joint degeneration. Specifically, miR-204/-211 loss-of-function induces matrix-degrading proteases in articular chondrocytes and synoviocytes, stimulating articular cartilage destruction. Moreover, miR-204/-211 ablation enhances NGF expression in a Runx2-dependent manner, and thus hyper-activates Akt signaling and MPC proliferation, underlying multiplex non-cartilaginous OA conditions including synovial hyperplasia, osteophyte outgrowth and subchondral sclerosis. Importantly, miR-204/-211-deficiency-induced OA is largely rescued by Runx2 insufficiency, confirming the miR-204/-211-Runx2 axis. Further, intraarticular administration of miR-204-expressing adeno-associated virus significantly decelerates OA progression. Collectively, miR-204/-211 are essential in maintaining healthy homeostasis of mesenchymal joint cells to counteract OA pathogenesis.

Indexed as

AnimalsChondrocytesCore Binding Factor Alpha 1 SubunitMesenchymal Stem CellsMiceMice, KnockoutMicroRNAsOsteoarthritisPeptide HydrolasesSynoviocytesCore Binding Factor Alpha 1 SubunitMicroRNAsMIRN204 microRNA, mouseMirn211 microRNA, mousePeptide HydrolasesRunx2 protein, mouse

Identifiers

PMID31253842
PMCPMC6599052
OpenAlexW2956122478

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.