Endothelial progenitor cell transplantation attenuates lipopolysaccharide-induced acute lung injury via regulating miR-10a/b-5p

被引：10

作者：

Jin, Yan ^{[1
]}

Yang, Chen ^{[1
]}

Sui, Xintong ^{[1
]}

Cai, Quan ^{[1
]}

Guo, Liang ^{[1
]}

Liu, Zhi ^{[1
]}

机构：

[1] China Med Univ, Dept Emergency, Affiliated Hosp 1, 155 Nanjing N St, Shenyang 110001, Liaoning, Peoples R China

来源：

LIPIDS IN HEALTH AND DISEASE | 2019年 / 18卷 / 1期

基金：

中国国家自然科学基金;

关键词：

Acute lung injury; Endothelial progenitor cells; microRNA; Cell transplantation; Neovascularization; PERMEABILITY;

D O I：

10.1186/s12944-019-1079-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

BackgroundBone marrow-derived endothelial progenitor cells (EPCs) are shown to attenuate lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in animal models. However, the molecular mechanism is largely unknown.Materials and methodsThe animal model of ALI was induced by intratracheal instillation of purified LPS with 2.5mg/ml/kg. The expression of microRNAs and ADAM15 in lung tissues and LPS-induced mouse pulmonary microvascular endothelial cells (MPMVECs) was determined by quantitative real-time PCR and western blot analysis. The target relationship between miR-10a/b-5p and ADAM15 was confirmed by luciferase reporter assay and RNA interference. The effect of EPCs on MPMVEC proliferation was detected by MTT assay.ResultsEPCs increased the expression of miR-10a/b-5p and reduced ADAM15 protein level in LPS-induced ALI lung tissues and MPMVECs (p<0.05), and promoted LPS-induced MPMVEC proliferation (p<0.05). ADAM15 was confirmed to be a downstream target of miR-10a/b-5p. Additionally, EPCs promoted LPS-induced MPMVEC proliferation and exerted the therapeutic effect of ALI via regulating miR-10a/b-5p/ADAM15 axis.ConclusionEPC transplantation exerted its therapeutic effect of ALI via increasing miR-10a/b-5p and reducing ADAM15, thus providing a novel insight into the molecular mechanism of EPC transplantation in treating ALI.

引用

页数：10

共 35 条

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