Exosomal miR-22-3p Derived from Chronic Rhinosinusitis with Nasal Polyps Regulates Vascular Permeability by Targeting VE-Cadherin

Abstract EN

Background.

The abnormal vascular permeability is associated with the formation of chronic rhinosinusitis with nasal polyps (CRSwNP).

Previously, our study demonstrated that the nasal lavage fluid- (NLF-) derived exosomes from CRSwNP can promote the vascular permeability of human umbilical vein endothelial cells (HUVECs).

miR-22-3p, a specific differentiated miRNA, is reported to regulate microvessels in some diseases.

This study is purposed to explore the impact of exosomal miR-22-3p derived from CRSwNP on vascular permeability and identify the underlying targets.

Methods.

Exosomes were extracted from NLF of 26 CRSwNP patients and 10 control patients.

Quantitative real-time PCR (qRT- PCR) was applied to evaluate the relative level of exosomal miR-22-3p.

The impact of exosomal miR-22-3p on HUVECs was assessed by permeability assays in vitro.

The potential molecular targets of miR-22-3p were investigated by applying such technologies as dual-luciferase reporter assay and western blot.

Results.

miR-22-3p was upregulated in NLF-derived exosomes from CRSwNP.

Exosomal miR-22-3p derived from CRSwNP enhanced the tubule permeability of HUVECs.

Vascular endothelial- (VE-) cadherin (CDH5) was identified as a direct target of miR-22-3p.

miR-22-3p regulated the vascular permeability by targeting VE-cadherin in HUVECs.

Conclusions.

Exosomal miR-22-3p derived from NLF of CRSwNP plays an important role in regulating vascular permeability by targeting VE-cadherin.