Evidence map›Paper›PMID 27023516›Full record

ArticleInternational journal of molecular sciences2016

Mechanical and IL-1β Responsive miR-365 Contributes to Osteoarthritis Development by Targeting Histone Deacetylase 4.

Xu Yang, Yingjie Guan, Shaoqi Tian, Yuanhe Wang, Kang Sun, Qian Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
12.3field-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

62 citing papers in PubMed, 90 citations in OpenAlex.

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2 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

6 authors at 3 institutions in 2 countries.

Xu YangDepartment of Orthopedics, the Affiliated Hospital of Qingdao University, 1677 Wutaishan Rd, Qingdao 266000, China. xu_yang0608@outlook.com.
Yingjie GuanCell and Molecular Biology Laboratory, Department of Orthopedics, Alpert Medical School of Brown University/Rhode Island Hospital, Providence, RI 02903, USA. yingjie_guan@brown.edu.
Shaoqi TianDepartment of Orthopedics, the Affiliated Hospital of Qingdao University, 1677 Wutaishan Rd, Qingdao 266000, China. shaoqi99@aliyun.com.
Yuanhe WangDepartment of Orthopedics, the Affiliated Hospital of Qingdao University, 1677 Wutaishan Rd, Qingdao 266000, China. wangyuanhe-2004@163.com.
Kang SunDepartment of Orthopedics, the Affiliated Hospital of Qingdao University, 1677 Wutaishan Rd, Qingdao 266000, China. kangsun1@outlook.com.
Qian ChenCell and Molecular Biology Laboratory, Department of Orthopedics, Alpert Medical School of Brown University/Rhode Island Hospital, Providence, RI 02903, USA. qian_chen@brown.edu.
Qingdao University · CNRhode Island Hospital · USAffiliated Hospital of Qingdao University · CN

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
NIGMS NIH HHS P20 GM104937
6 · The paper itself

Abstract

Mechanical stress plays an important role in the initiation and progression of osteoarthritis. Studies show that excessive mechanical stress can directly damage the cartilage extracellular matrix and shift the balance in chondrocytes to favor catabolic activity over anabolism. However, the underlying mechanism remains unknown. MicroRNAs (miRNAs) are emerging as important regulators in osteoarthritis pathogenesis. We have found that mechanical loading up-regulated microRNA miR-365 in growth plate chondrocytes, which promotes chondrocyte differentiation. Here, we explored the role of the mechanical responsive microRNA miR-365 in pathogenesis of osteoarthritis (OA). We found that miR-365 was up-regulated by cyclic loading and IL-1β stimulation in articular chondrocytes through a mechanism that involved the transcription factor NF-κB. miR-365 expressed significant higher level in rat anterior cruciate ligament (ACL) surgery induced OA cartilage as well as human OA cartilage from primary OA patients and traumatic OA Patients. Overexpression of miR-365 in chondrocytes increases gene expression of matrix degrading enzyme matrix metallopeptidase 13 (MMP13) and collagen type X (Col X). The increase in miR-365 expression in OA cartilage and in response to IL-1 may contribute to the abnormal gene expression pattern characteristic of OA. Inhibition of miR-365 down-regulated IL-1β induced MMP13 and Col X gene expression. We further showed histone deacetylase 4 (HDAC4) is a direct target of miR-365, which mediates mechanical stress and inflammation in OA pathogenesis. Thus, miR-365 is a critical regulator of mechanical stress and pro-inflammatory responses, which contributes cartilage catabolism. Manipulation of the expression of miR-365 in articular chondrocytes by miR-365 inhibitor may be a potent therapeutic target for the prevention and treatment of osteoarthritis.

Indexed as

AgedAnimalsCartilage, ArticularCells, CulturedChondrocytesDown-RegulationFemaleHistone DeacetylasesHumansInterleukin-1betaMaleMatrix Metalloproteinase 13MicroRNAsMiddle AgedNF-kappa BOsteoarthritisHDAC4 protein, humanHistone DeacetylasesInterleukin-1betaMatrix Metalloproteinase 13MicroRNAsMIRN365 microRNA, humanNF-kappa BRepressor Proteinsinflammationmechanical loadingmiR-365osteoarthritis

Identifiers

PMID27023516
PMCPMC4848892
OpenAlexW2309057421

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.