Abstract
Background: The occurrence
of nasal polyps is related to mucosal barrier damage. The role of MG53,
an important epithelial repair regulator, in nasal polyps remains
unclear. This study aimed to investigate the role of MG53 in nasal
epithelial repair.
Methods: We divided the patients into the following three
groups (n=15 each): chronic rhinosinusitis without nasal polyps
(CRSsNP), chronic rhinosinusitis with nasal polyps (CRSwNP) and septal
deviation (control). We performed qRT-PCR and western blotting to
determine the expression of MG53, TGF-β1, Smad2/3, zonula occluden-1
(ZO-1), and collagen-a1 (Col-a1) in nasal tissues and human nasal
epithelial cells (HNECs). HNECs were cultured to investigate the
regulatory role of MG53 and the TGF-β1/Smad pathway in the repair of
nasal epithelial cells.
Results: We found that the expression of MG53, TGF-β1, Smad2/3,
ZO-1, and Col-a1 was upregulated in the CRSsNP group, whereas it was
downregulated in the CRSwNP group. In the HNECs of nasal polyps, the
expression of TGF-β1, Smad2/3, ZO-1, and Col-a1 was downregulated after
overexpressed MG53, whereas this was reversed by the knockdown of MG53.
Additionally, we found that TGF-β1 stimulation resulted in significantly
upregulated MG53 expression, which was impeded by TGF-β1 inhibitors.
MG53 expression facilitated proliferation, promoted the secretion of
Col-a1, and inhibited apoptosis in HNECs.
Conclusion: MG53 inhibited the TGF-β1/Smad pathway and
fibrosis, enhanced the proliferation of nasal epithelial cells, and
supported nasal epithelial repair. The results of this study provide a
new therapeutic regimen for the treatment of nasal polyps.
Keywords: epithelial repair; mitsugumin53; nasal polyps; tight
junction; TGF-β1/Smad.