Evidence map›Paper›PMID 28471382›Full record

ArticleInternational journal of molecular sciences2017

Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway.

Yong Wang, Tao Yang, Yadong Liu, Wei Zhao, Zhen Zhang, Ming Lu, Weiguo Zhang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Yong WangDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. WY_landy1116@163.com.
Tao YangDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. yangtao_07@126.com.
Yadong LiuDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. doctoryadong@163.com.
Wei ZhaoThe 4th Department of Orthopedic Surgery, The Central Hospital Affiliated to Shenyang Medical College, Shenyang 110024, China. zhaowei332@126.com.
Zhen ZhangDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. doctorzz@126.com.
Ming LuDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. dllm@2008.sina.com.
Weiguo ZhangDepartment of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. zhangweiguo@dum.edu.cn.
Dalian Medical University · CNCentral Hospital Affiliated to Shenyang Medical College · CNFirst Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Slow growth and rapid loss of chondrogenic phenotypes are the major problems affecting chronic cartilage lesions. The role of microRNA-195 (miR-195) and its detailed working mechanism in the fore-mentioned process remains unknown. Fibroblastic growth factor 18 (FGF-18) plays a key role in cartilage homeostasis; whether miR-195 could regulate FGF-18 and its downstream signal pathway in chondrocyte proliferation and maintenance of chondrogenic phenotypes still remains unclear. The present research shows elevated miR-195 but depressed FGF-18 expressed in joint fluid specimens of 20 patients with chronic cartilage lesions and in CH1M and CH3M chondrocytes when compared with that in joint fluid specimens without cartilage lesions and in CH1W and CH2W chondrocytes, respectively. The following loss of function test revealed that downregulation of miR-195 by transfection of miR-195 inhibitors promoted chondrocyte proliferation and expression of a type II collagen α I chain (Col2a1)/aggrecan. Through the online informatics analysis we theoretically predicted that miR-195 could bind to a FGF-18 3' untranslated region (3'UTR), also, we verified that a miR-195 could regulate the FGF-18 and its downstream pathway. The constructed dual luciferase assay further confirmed that FGF-18 was a direct target of miR-195. The executed anti-sense experiment displayed that miR-195 could regulate chondrocyte proliferation and Col2a1/aggrecan expression via the FGF-18 pathway. Finally, through an in vivo anterior cruciate ligament transection (ACLT) model, downregulation of miR-195 presented a significantly protective effect on chronic cartilage lesions. Evaluating all of the outcomes of the current research revealed that a decrease of miR-195 protected chronic cartilage lesions by promoting chondrocyte proliferation and maintenance of chondrogenic phenotypes via the targeting of the FGF-18 pathway and that the miR-195/FGF-18 axis could be a potential target in the treatment of cartilage lesions.

Indexed as

Cell Proliferation3' Untranslated RegionsAggrecansAnimalsCase-Control StudiesCells, CulturedChondrocytesChondrogenesisCollagen Type IIFemaleFibroblast Growth FactorsHEK293 CellsHumansMicroRNAsOsteochondritisPhenotype3' Untranslated RegionsAggrecansCollagen Type IIfibroblast growth factor 18Fibroblast Growth FactorsMicroRNAsMIRN195 microRNA, humancartilage lesionchondrocyte proliferationCol2a1/aggrecanFGF18miR-195signal pathway

Identifiers

PMID28471382
PMCPMC5454888
OpenAlexW2611044407

What OpenQuestion holds

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Registered trials

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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.