Evidence map›Paper›PMID 31702033›Full record

ArticleMolecular medicine reports2019

MicroRNA‑186‑5p mediates osteoblastic differentiation and cell viability by targeting CXCL13 in non‑traumatic osteonecrosis.

Weihua Xu, Jin Li, Hongtao Tian, Ruoyu Wang, Yong Feng, Jing Tang, Jie Jia

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. 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

7 authors at 2 institutions in 1 country.

Weihua XuDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Jin LiDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Hongtao TianDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Ruoyu WangDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Yong FengDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Jing TangCancer Centre, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Jie JiaDepartment of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRs) serve varying and important roles in the pathogenesis of non‑traumatic osteonecrosis (ON). However, the role miR‑186‑5p serves in the pathogenesis of osteonecrosis remains unknown and the clinical outcome of ON is still uncertain. The aim of the present study was to determine the expression characteristics, biological function and molecular mechanisms of miR‑186‑5p, which is associated with cancer development and progression, in osteoblastic differentiation and cell viability. The results of the present study showed that the expression levels of miR‑186‑5p were significantly higher in clinical non‑traumatic ON compared with osteoarthritis samples (P=0.0001). An inverse association was observed between miR‑186‑5p and CXCL13 expression levels. Furthermore, miR‑186‑5p inhibited phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling, downregulated osteoblast‑specific markers and reduced the viability and differentiation of human mesenchymal stem cells from bone marrow (HMSC‑bm) through targeting CXCL13. Increasing expression of CXCL13 in HMSC‑bm cells partially restored miR‑186‑5p‑mediated inhibition. In conclusion, abrogation of PI3K/AKT signaling triggered by miR‑186‑5p/CXCL13 may contribute to ON pathogenesis. These results highlight the possible clinical value of miR‑186‑5p in treatment for non‑traumatic ON.

Indexed as

Cell DifferentiationCell SurvivalCell LineChemokine CXCL13FemaleHumansMaleMAP Kinase Signaling SystemMicroRNAsMiddle AgedOsteoblastsOsteonecrosisChemokine CXCL13CXCL13 protein, humanMicroRNAsMIRN186 microRNA, human

Identifiers

PMID31702033
PMCPMC6797973
OpenAlexW2975560048

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.