Evidence map›Paper›PMID 31050590›Full record

ArticlePrion2019

Enrichment of miR-126 enhances the effects of endothelial progenitor cell-derived microvesicles on modulating MC3T3-E1 cell function via Erk1/2-Bcl-2 signalling pathway.

Guanghua Chen, Peng Li, Zhijun Liu, Rong Zeng, Xiaotang Ma, Yanfang Chen, Haijia Xu, Zhanghua Li, Hao Lin

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Prion, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. [Application of Extracellular Vesicles Derived from Vascular Endothelial/Endothelial Progenitor Cells in Tissue Regeneration and Repair].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022
    Review
  5. Article
  6. Review
  7. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Guanghua Chena Department of Orthopedics, The First Clinical Medical College , Jinan University , Guangzhou , China.
Peng Lib Department of Orthopedics , Affiliated Hospital of Guangdong Medical University , Zhanjiang , China.
Zhijun Liub Department of Orthopedics , Affiliated Hospital of Guangdong Medical University , Zhanjiang , China.
Rong Zengb Department of Orthopedics , Affiliated Hospital of Guangdong Medical University , Zhanjiang , China.
Xiaotang Mac Department of Surgery , Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University , Zhanjiang , China.
Yanfang Chend Department of Pharmacology & Toxicology, Boonshoft School of Medicine , Wright State University , Dayton , OH , USA.
Haijia Xue Department of Orthopedics , Tongren Hospital of Wuhan University , Wuhan , China.
Zhanghua Lie Department of Orthopedics , Tongren Hospital of Wuhan University , Wuhan , China.
Hao Linb Department of Orthopedics , Affiliated Hospital of Guangdong Medical University , Zhanjiang , China.
Guangdong Medical College · CNTongren Hospital · CNWright State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo evaluate whether EPC-MVs could promote bone regeneration by directly regulating osteoblast through miR-126. The underlying mechanisms were also explored.

methodsEPCs were isolated from bone marrow mononuclear cells. EPC-MVs were collected from EPCs cultured medium. The lentivirus was used to induce miR-126 over-expression in EPCs and EPC-MVs. miR-126 expression was detected by qRT-PCR. The proliferation, migration, apoptosis and differentiation abilities of osteoblast cells MC3T3-E1 were analysed in the presence or absence of EPC-MVs or miR-126 overexpressed EPC-MVs (EPC-MVs-miR126). The proteins of Erk1/2 and Bcl-2 were analysed by western blot. Erk1/2 inhibitor was used for pathway exploration.

resultsEPC-MVs reduced apoptosis and promoted proliferation and migration of MC3T3-E1 cells, which could be enhanced by miR-126 enrichment (p< 0.05). Neither EPC-MVs nor EPC-MVs-miR126 had an effect on MC3T3-E1 cell osteogenic differentiation (p> 0.05). EPC-MVs-miR126 had better effects than EPC-MVs on upregulating the expressions of p-Erk1/2 and Bcl-2, which were abolished by Erk1/2 inhibitor. ERK1/2-Bcl-2 activity plays a crucial role in the regulation of EPC-MVs/EPC-MVs-miR126 on the effect of MC3T3-E1 cells.

conclusionEPC-MVs promote proliferation and migration of MC3T3-E1 cell while reduced apoptosis via the miR-126/Erk1/2-Bcl-2 pathway. A combination of EPC-MVs and miR-126 might provide novel therapeutic targets for bone regeneration and fracture healing through regulating osteoblast.

Indexed as

MAP Kinase Signaling SystemAnimalsApoptosisCell-Derived MicroparticlesCell DifferentiationCell LineCell ProliferationCells, CulturedCell SurvivalEndothelial Progenitor CellsMaleMiceMice, Inbred C57BLMicroRNAsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mapk1 protein, mouseMicroRNAsMIRN126 microRNA, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2Endothelial progenitor cellsmicrovesiclesmiR-126osteoblasts

Identifiers

PMID31050590
PMCPMC7000145
OpenAlexW2943704426

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.