Abstract
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.
Highlights
Chronic rhinosinusitis (CRS) is characterized by the chronic inflammation of the paranasal sinus mucosa that persists for at least 12 weeks [1]
Exosomal lipid bilayer membranes were observed under transmission electron microscopy (TEM), which confirmed the presence of exosomes in the morphology (Figures 1(a) and 1(b))
After a series of cellular analyses, we found that the upregulation of miR-22-3p enhanced the vascular permeability of human umbilical vein endothelial cells (HUVECs), while silencing miR-22-3p expression inhibited the function (Figure 2(f))
Summary
Chronic rhinosinusitis (CRS) is characterized by the chronic inflammation of the paranasal sinus mucosa that persists for at least 12 weeks [1]. The abnormal vascular permeability is associated with the formation of chronic rhinosinusitis with nasal polyps (CRSwNP). 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). This study is purposed to explore the impact of exosomal miR22-3p derived from CRSwNP on vascular permeability and identify the underlying targets. The impact of exosomal miR-22-3p on HUVECs was assessed by permeability assays in vitro. Exosomal miR22-3p 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
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