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September 14, 2020Cardiology Research and PracticeOpen Access

Upregulation of MicroRNA-125b Leads to the Resistance to Inflammatory Injury in Endothelial Progenitor Cells

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Why the study?

MicroRNA-125b regulates inflammatory responses in cardiovascular diseases, but its role in modulating endothelial progenitor cell function in ischemic hearts remained unclear.

Does miR-125b overexpression improve endothelial progenitor cell function and cardiac recovery in a myocardial infarction model?

Population

Cultured endothelial progenitor cells and a mouse myocardial infarction model

Comparison

Transfection with miR-125b mimic vs negative control mimic

Design

In vitro cell study and in vivo preclinical animal model

Authors

KYKe YangXLXing LiuWLWanwen Lin

Discussion

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Member takes

Overview

miR-125b may modulate EPC function in TNF-α inflammation; leaves open therapeutic targeting in ischemic heart disease.

Structured PICO

Does miR-125b overexpression improve endothelial progenitor cell function and cardiac recovery in a myocardial infarction model?

P
Population
Endothelial progenitor cells (EPCs) in vitro and a mouse myocardial infarction model in vivo
I
Intervention
miR-125b overexpression (transfection with miR-125b mimic)
C
Comparator
Negative control (NC) mimic
O
Outcome
Cell migration, adhesion, apoptosis, NF-κB pathway activation, cardiac function recovery, and capillary vessel densitysurrogate

Upregulation of miR-125b protects endothelial progenitor cells against inflammatory injury and improves their ability to mediate neovascularization and cardiac repair after myocardial infarction.

Cite This Study

Yang et al. (2020) studied this question.

synapsesocial.com/papers/6a6fe8a375498292b70949echttps://doi.org/10.1155/2020/6210847
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