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MiR-106b exhibits an anti-angiogenic function by inhibiting STAT3 expression in endothelial cells

Overview of attention for article published in Lipids in Health and Disease, March 2016
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Title
MiR-106b exhibits an anti-angiogenic function by inhibiting STAT3 expression in endothelial cells
Published in
Lipids in Health and Disease, March 2016
DOI 10.1186/s12944-016-0216-5
Pubmed ID
Authors

Ailifeire Maimaiti, Aikebaier Maimaiti, Yining Yang, Yitong Ma

Abstract

Recent discoveries of the atherosclerosis-related miRNAs shed new light on the treatment of cardiovascular diseases. Of note, miR-106b ~ 25 cluster and miR-17 ~ 92 cluster are paralogs. Up till now, plenty of researches have shown the role of miR-17 ~ 92 cluster in tumor and atherosclerosis, but miR-106b ~ 25 cluster has stayed mysterious in atherosclerosis field. This study was designed to investigate how miR-106b functions in the atherosclerosis-related angiogenesis and to explore the functioning processes of miR-106b, so as to seek out a new target for the treatment of atherosclerosis. Up and down regulation of miR-106b expression was achieved through transfection in HUVECs so as to investigate the function of miR-106b. Next we predicted the target genes of miR-106b and detected them using qRT-PCR and Western blot technique. At last, luciferase assay was conducted to verify the direct target gene of miR-106b. Data are expressed as mean ± SEM. Two treatment groups were compared by Mann-Whitney U test or student's t-test. Results were considered statistically significant when P < 0.05. The results showed miR-106b up-regulation groups formed less tubes than control groups while the down-regulation groups showed the opposite. Meanwhile, no obvious effect on apoptosis was observed in endothelial cells. Next we predicted the target genes of miR-106b and finally settled down to MAPK14 (Mitogen-Activated Protein Kinase), STAT3 (Signal Transducers and Activators of Transcription 3), JAK1(Janus Kinase 1) and VEGFA(Vascular Endothelial Growth Factor A) as candidate target genes. Our results revealed over-expressed miR-106b represses STAT3 expression, while miR-106b inhibition resulted in STAT3 up-regulation. Ultimately, luciferase assay confirmed STAT3 mRNA is the direct target of miR-106b. Our research demonstrated that miR-106b modulate angiogenesis in endothelial cells through affecting expression of STAT3, which occurs by direct target action. Therefore, we affirmed that miR-106b exerts an anti-angiogenic effect in endothelial cells via STAT3-involved signaling pathway, via directly targeting STAT3.

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Mendeley readers

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The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 26%
Student > Ph. D. Student 6 22%
Student > Master 3 11%
Student > Bachelor 2 7%
Professor 1 4%
Other 2 7%
Unknown 6 22%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 33%
Medicine and Dentistry 4 15%
Agricultural and Biological Sciences 2 7%
Immunology and Microbiology 2 7%
Social Sciences 1 4%
Other 2 7%
Unknown 7 26%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 10 March 2016.
All research outputs
#20,315,221
of 22,856,968 outputs
Outputs from Lipids in Health and Disease
#1,202
of 1,448 outputs
Outputs of similar age
#253,440
of 300,116 outputs
Outputs of similar age from Lipids in Health and Disease
#30
of 35 outputs
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So far Altmetric has tracked 1,448 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.0. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 35 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.