丹麦克朗
Wnt信号通路
小RNA
基因敲除
急性呼吸窘迫综合征
间充质干细胞
癌症研究
流式细胞术
下调和上调
干细胞
生物
免疫学
医学
分子生物学
细胞生物学
肺
信号转导
内科学
细胞培养
基因
遗传学
出处
期刊:PubMed
日期:2018-07-01
卷期号:22 (14): 4625-4633
被引量:13
标识
DOI:10.26355/eurrev_201807_15521
摘要
To explore whether microRNA-615-3p participates in the progression of neonatal acute respiratory distress syndrome (ARDS) by inhibiting differentiation of mesenchymal stem cells (MSCs) to alveolar type II epithelial cells (ATII) via Wnt/β-catenin pathway.Expression levels of microRNA-615-3p and inflammatory factors (IL-1, IL-6, IL-8, and TNF-α) in peripheral blood of 24 neonatal ARDS patients and 14 healthy newborns were detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction). MSCs were isolated from bone marrow of mice and identified by flow cytometry. The effect of microRNA-615-3p on regulating the differentiation of MSCs to ATII was analyzed. After altering expressions of microRNA-615-3p and DKK1 by plasmids transfection, Wnt/β-catenin pathway-related genes were detected by Western blot.Higher expression levels of microRNA-615-3p and inflammatory factors (IL-1, IL-6, IL-8, and TNF-α) were observed in peripheral blood of neonatal ARDS patients than those of healthy newborns. ATII-specific genes were upregulated, and inflammatory factors were downregulated after the microRNA-615-3p knockdown in MSCs. Moreover, expressions of Wnt/β-catenin pathway-related genes were downregulated after the microRNA-615-3p overexpression, which was partially reserved by the DKK1 knockdown.Overexpressed microRNA-615-3p promoted ARDS development through inhibiting differentiation of MSCs to ATII via Wnt/β-catenin pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI