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MiR-320 regulates cardiomyocyte apoptosis induced by ischemia–reperfusion injury by targeting AKIP1

Overview of attention for article published in Cellular & Molecular Biology Letters, August 2018
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Title
MiR-320 regulates cardiomyocyte apoptosis induced by ischemia–reperfusion injury by targeting AKIP1
Published in
Cellular & Molecular Biology Letters, August 2018
DOI 10.1186/s11658-018-0105-1
Pubmed ID
Authors

Zhi-Qiang Tian, Hong Jiang, Zhi-Bing Lu

Abstract

MicroRNAs play important roles in regulation of the cardiovascular system. The purpose of this study was to investigate microRNA-320 (miR-320) expression in myocardial ischemia-reperfusion (I/R) injury and the roles of miR-320 in cardiomyocyte apoptosis by targeting AKIP1 (A kinase interacting protein 1). The level of miR-320 was detected using quantitative real-time polymerase chain reaction (qRT-PCR), and cardiomyocyte apoptosis was detected via terminal dUTP nick end-labeling assay. Cardiomyocyte apoptosis and the mitochondrial membrane potential were evaluated via flow cytometry. Bioinformatics tools were used to identify the target gene of miR-320. The expression levels of AKIP1 mRNA and protein were detected via qRT-PCR and Western blot, respectively. Both the level of miR-320 and the rate of cardiomyocyte apoptosis were substantially higher in the I/R group and H9c2 cells subjected to H/R than in the corresponding controls. Overexpression of miR-320 significantly promoted cardiomyocyte apoptosis and increased the loss of the mitochondrial membrane potential, whereas downregulation of miR-320 had an opposite effect. Luciferase reporter assay showed that miR-320 directly targets AKIP1. Moreover, knock down and overexpression of AKIP1 had similar effects on the H9c2 cells subjected to H/R. miR-320 plays an important role in regulating cardiomyocyte apoptosis induced by I/R injury by targeting AKIP1 and inducing the mitochondrial apoptotic pathway.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 20%
Student > Doctoral Student 3 15%
Student > Bachelor 2 10%
Student > Postgraduate 2 10%
Professor > Associate Professor 2 10%
Other 1 5%
Unknown 6 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 25%
Medicine and Dentistry 4 20%
Neuroscience 3 15%
Materials Science 1 5%
Unknown 7 35%

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 28 August 2018.
All research outputs
#10,685,593
of 13,434,786 outputs
Outputs from Cellular & Molecular Biology Letters
#97
of 225 outputs
Outputs of similar age
#199,362
of 266,657 outputs
Outputs of similar age from Cellular & Molecular Biology Letters
#1
of 1 outputs
Altmetric has tracked 13,434,786 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 225 research outputs from this source. They receive a mean Attention Score of 2.1. This one is in the 16th percentile – i.e., 16% of its peers scored the same or lower than it.
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