Gludwarming2378

This study aims to investigate the regulatory role of exosome lncRNA OIP5-AS1 in tumor progression and autophagy.

Seventy-three cases of osteosarcoma (OS) tissues and 56 cases of adjacent normal tissues were collected to culture human OS cell line HOS. Ilginatinib datasheet The exosomes secreted by OS cell line were isolated and collected. Apoptosis and exosome markers were detected by flow cytometry. A nude mouse model of OS was established. The gene expression levels of lncRNA OIP5-AS1, miR-153 and autophagy-related protein 5 (ATG5) were quantified by real-time quantitative PCR (RT-PCR). The binding sites of lncRNA OIP5-AS1 and miR-153 were predicted by Starbase3.0, and the binding sites of miR-153 and ATG5 were predicted by Targetscan7.2. The gene binding sites were verified by luciferase reporter gene detection or RNA immunoprecipitation (RIP). The relative level of protein was tested by Western blot. Transwell was applied to test migration and invasion of OS cells. The angiogenesis of OS cells was tested by tubule formatinesis level caused by the exosomal lncRNA OIP5-AS1, which was then reversed by the increase of miR-153 and decrease of ATG5.

Highly enriched exosomal lncRNA OIP5-AS1 can regulate OS tumor angiogenesis and autophagy through miR-153 and ATG5.

Highly enriched exosomal lncRNA OIP5-AS1 can regulate OS tumor angiogenesis and autophagy through miR-153 and ATG5.

Spontaneous abortion (SA) is a common complication in early pregnancy. Nevertheless, SA's etiology is complex, and the underlying molecular mechanisms of the pathogenesis behind SA remains unclear. The present study aims to find the feasibility of using serum exosomal miRNAs as novel biomarkers for SA.

In our study, we isolated the serum exosomes from the peripheral blood of the subjects. Then transmission electron microscopy (TEM), WB, and in vitro exosome tracing experiments were used. Comprehensive exosomal miRNA sequencing was performed to profile the differentially expressed miRNAs between the SA and normal pregnancy groups. Furthermore, genes targeted by miRNAs were further predicted and verified by TargetScan, miRDB, miRTarBase, miRWalk and HMDD V3.2. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and pathway category were performed by the DIANA-miRPath v3.0 online tool. We then validated the expression levels of selected miRNAs by qRT-PCR. ROC analysis was performed to explore themiRNAs from exosomes are altered in patients with SA. Findings of this exploratory study may provide potential biomarkers for SA.

Our results suggest that the circulating miRNAs from exosomes are altered in patients with SA. Findings of this exploratory study may provide potential biomarkers for SA.The relevance of stem cell-derived exosomes has been implicated in necrotizing enterocolitis, while the involvement of serum-derived exosomes from children with Hirschsprung-associated enterocolitis (HAEC) in pathogenesis of HAEC remains unclear. This study set to identify the roles of exosomal microRNA (miR)-18a-5p from sera of HAEC patients in human-derived colonic epithelial NCM460 cells and in mice with HAEC. Exosomes were isolated from the sera of healthy children (Healthy-exo), patients with Hirschsprung's disease (HSCR) (HSCR-exo) or HAEC (HAEC-exo). A microarray analysis of miRNAs was implemented to assess the enrichment of miRNAs in these exosomes. HAEC-exo was significantly enriched in miR-18a-5p. HAEC-exo led to the generation of a pro-inflammatory microenvironment, inhibition of cellular DNA synthesis, and promotion of apoptosis in NCM460 cells. Mechanistically, miR-18a-5p targeted and repressed retinoid-related orphan receptor α (RORA) expression, thereby regulating the Sirtuin 1 (SIRT1)/nuclear factor-kappa B (NFκB) pathway. Overexpression of RORA ameliorated inflammatory damage in NCM460 cells caused by exosomal miR-18a-5p. HAEC-exo exacerbated inflammatory damage in HAEC mice, and this facilitation was reversed after RORA overexpression. Collectively, exosomal miR-18a-5p was a promoter of HAEC, which induces the intestine cell apoptosis and inflammatory responses through the inhibition of SIRT1/NFκB pathway by targeting RORA.

To explore the effect of exosomes containing miR-122-5p secreted by lipopolysaccharide (LPS)-induced neutrophils on the apoptosis and permeability of brain microvascular endothelial cells (BMECs).

Neutrophils in blood were isolated, purified and identified. LPS-induced neutrophils were co-cultured with BMECs. Untreated or LPS-induced neutrophil exosomes were isolated and identified with a transmission electron microscope. miR-122-5p expressions in the exosomes were detected by real-time quantitative polymerase chain reaction, and then the exosomes were co-cultured with BMECs. Bioinformatics analysis was performed to predict the downstream target gene of miR-122-5p, and OCLN was selected as the subject. Dual luciferase reporter assay was carried out to verify the interactive relationship between OCLN and miR-122-5p. LPS and miR-122-5p were used to treat neutrophils, and then exosomes were collected. Exosome or OCLN was embedded in BMECs. The proliferation, colony forming ability and apoptosis of BMECs weren of OLCN expression can aggravate BMECs injury.Esophageal squamous cell carcinoma (ESCC) increases at fast rate of all cancer types in China, which urges the investigations of its potential mechanism. In this research, a highly expressed kinesin superfamily protein 22 (KIF22) was founded both in ESCC tissues and cancer cell lines. The following experiments pointed out that down-regulation of KIF22 remarkably restrained the malignant progression of ESCC cells. Besides, KIF22 knockdown promoted ESCC cells apoptosis and arrested cells in G0/G1 phase, while KIF22 also regulated the expression of cell cycle- and EMT-related proteins. Previous research revealed that the aberrant expressions of microRNAs (miRNAs) are related to tumors development. Based on the predict result, KIF22 was considered as the target of miR-122, which was demonstrated by luciferase reporter assay. miR-122 inhibitor could significantly reverse the function of KIF22 knockdown, including cell proliferation, migration and invasion. Furthermore, down-expressed miR-122 altered the function of KIF22 knockdown on cell cycle- and EMT-related proteins.