生物
滋养层
细胞凋亡
免疫印迹
小RNA
荧光素酶
细胞生物学
流式细胞术
MMP9公司
脂质体
转染
免疫学
胎盘
细胞培养
下调和上调
载体(分子生物学)
胎儿
基因
遗传学
怀孕
重组DNA
作者
Yi Chen,Cheng Yu,Fengli Hu,Yanmin Zhu,Xie Xiu-qin
出处
期刊:Tissue & Cell
[Elsevier BV]
日期:2022-05-20
卷期号:77: 101827-101827
被引量:4
标识
DOI:10.1016/j.tice.2022.101827
摘要
When the abnormality occurs in proliferation, differentiation and apoptosis of trophoblasts, the invasion ability of placental trophoblast is weakened, which is prone to trigger the occurrence of various pregnancy diseases such as repeated spontaneous abortion (RSA). Clinically, Astragalus and Codonopsis pilosula polysaccharides (APS and CPPS) are used for the treatment of unexplained recurrent spontaneous abortion (URSA). Therefore, we aimed to probe into the roles of APS and CPPS in biological behaviors of placental trophoblasts. The trophoblasts were treated with APS and CPPS, and transfected with miR-92a-1–5p mimic and CCR7 plasmid to explore the roles of APS and CPPS. Cell viability and apoptosis were determined by CCK-8 and flow cytometry, respectively. The levels of miRNA/mRNA and protein were measured by qRT-PCR and western blot, respectively. The interaction between miR-92a-1–5p and CCR7 was analyzed by TargetScan and dual-luciferase reporter assay. Invasion and migration rates were assessed by Transwell and wound healing assays, respectively. APS combined with CPPS enhanced viability, Bcl-2 expression, and migration and invasion capabilities, while suppressing apoptosis, and expressions of Bax, Bim and miR-92a-1–5p in trophoblasts. Nevertheless, miR-92a-1–5p mimic produced the inverse modulations in trophoblasts, and partially reversed the effects of APS and CPPS. Furthermore, overexpression of CCR7, the target of miR-92a-1–5p, partially offset the effect of miR-92a-1–5p mimic in trophoblasts. Astragalus combined with Codonopsis pilosula polysaccharides modulates the biological behaviors of trophoblasts via miR-92a-1–5p/CCR7 axis. The regulatory axis we studied will be helpful for the treatment of URSA in the future. • APS combined with CPPS increased the viability while suppressed miR-92a-1–5p expression of trophoblast. • MiR-92a-1–5p overexpression was offset the effects of APS combined with CPPS in trophoblast. • CCR7 was the target of miR-92a-1–5p.
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