LncRNA SND1-IT1 delivered via intracerebral hemorrhage-derived exosomes affect the growth of human microglia by regulating the miR-124-3p/MTF1 axis.

Abstract

In this study, we investigated the effects of long noncoding RNA (lncRNA) SND1-IT1 on human microglia (HMC3 cells) delivered by intracerebral hemorrhage (ICH)-derived exosomes (ICH-exos) as well as a competitive endogenous RNA (ceRNA) network. Exosomes obtained from ICH plasma were characterized by nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM), and western blot. RNA sequencing was performed to study the lncRNA transcriptome from ICH-exos and the healthy control-derived exosomes (HC-exos) and differentially expressed lncRNAs (DE-lncRNAs) were identified. HMC3 cells were treated with ICH-exos or transfected with pcDNA3.1-SND1-IT1, and then cell viability and apoptosis were measured. The ceRNA network (lncRNA SND1-IT1/miR-124-3p/messenger RNA MTF1) was chosen for further investigation. NTA, TEM, and western blot showed that exosomes were successfully separated and could be absorbed by HMC3 cells. The expression of lncRNA SND1-IT1 in ICH-exos was significantly higher than that of HC-exos (p < 0.05). In addition, lncRNA SND1-IT1 overexpression and ICH-exos significantly inhibited cell viability and enhanced apoptosis. A total of 162 DE-lncRNAs were identified by sequencing, and a ceRNA network was constructed. The dual-luciferase reporter gene indicated that lncRNA SND1-IT1, miR-124-3p, and MTF1 interacted with each other. Cell experiments showed that lncRNA SND1-IT1 affected the growth of HMC3 cells through miR-124-3p/MTF1. In conclusion, ICH-exos delivered lncRNA SND1-IT1 to HMC3 cells, and exosomal lncRNA SND1-IT1 can regulate cell viability and apoptosis to influence HMC3 cell growth via the SND1-IT1/miR-124-3p/MTF1 axis.