Acta parasitologica · 2025
The Effects of Extracellular Vesicles Derived from Hydatid Cyst Fluid on the Expression of microRNAs Involved in Liver Fibrosis.
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Mohammad Rahimi Hanieh, Mahdavi Fatemeh, Eslami Nasim, Nemati Sara, Mirjalali Hamed
Аннотация
INTRODUCTION: Hydatidosis is a zoonotic neglected disease caused by the larval stage of Echinococcus granulosus. Evidence suggests a communication between hydatid cyst (HC) and hosts via extracellular vesicles (EVs). However, a little is known about the communication between EVs derived from HC fluid (HCF) and host cells. The current study aimed to investigate the effect of HCF derived EVs on expression of fibrotic and anti-fibrotic miRNAs in THP-1 cell line.
METHODS: In the current study, EVs were isolated using ultracentrifugation from wild-infected sheep HCF and characterized by western blot, electron microscope, and size distribution analysis. The effects of EVs on the expression levels of microRNAs (mir-16, mir-29a, and mir-155) involved in liver fibrosis were investigated using quantitative real-time PCR (qRT-PCR), 3 and 24 h after incubation.
RESULTS: Western blot analyses confirmed the expression of CD63 marker, while Calnexin and CD81 were absent in EVs samples. The SEM and morphology revealed round shape vesicles. The DLS analysis showed average size distribution 130.6 nm diameter. The expression levels of mir-16 and mir-29a were significantly upregulated after 3 h for 8.66 and 3.420, respectively, while they were significantly downregulated after 24 h for 3.853 and 1.859, respectively.
CONCLUSION: The main mechanism of the communication between EVs derived from HCF and their host remains unclear. Our results suggest that HC may modulate the expression of miRNAs, involved in liver fibrosis via EVs.
METHODS: In the current study, EVs were isolated using ultracentrifugation from wild-infected sheep HCF and characterized by western blot, electron microscope, and size distribution analysis. The effects of EVs on the expression levels of microRNAs (mir-16, mir-29a, and mir-155) involved in liver fibrosis were investigated using quantitative real-time PCR (qRT-PCR), 3 and 24 h after incubation.
RESULTS: Western blot analyses confirmed the expression of CD63 marker, while Calnexin and CD81 were absent in EVs samples. The SEM and morphology revealed round shape vesicles. The DLS analysis showed average size distribution 130.6 nm diameter. The expression levels of mir-16 and mir-29a were significantly upregulated after 3 h for 8.66 and 3.420, respectively, while they were significantly downregulated after 24 h for 3.853 and 1.859, respectively.
CONCLUSION: The main mechanism of the communication between EVs derived from HCF and their host remains unclear. Our results suggest that HC may modulate the expression of miRNAs, involved in liver fibrosis via EVs.