Search

Photochromic hexaarylbiimidazoles (HABIs) enable reversible transformation between HABI and triphenylimidazole radicals (TPIRs) upon UV light irradiation, which have been applied in photo-patterning, super-resolution imaging, photoinduced self-healing materials and photomechanical hydrogels. Here, we designed and prepared a novel kind of polyurethane (PU) photoresist based on photo-cleavable HABI cross-linkers (HABI-PU), linear PU backbone and additive tert-butylhydroquinone (TBHQ) radical quencher. Upon UV light irradiation, the C-N bond inside HABI unit is broken, causing the transformation of HABI into two TPIRs which are subsequently quenched by TBHQ. Therefore, the cross-linking points of HABI-PU in UV irradiation area were broken, forming flexible PU polymer chains with declined molecular weight, which can be dissolved in developer. HABI-PU films show excellent photosensitivity as a positive photoresist in photolithography. The reaction mechanism between HABI and TBHQ was studied by UV-vis absorption spectra, electron paramagnetic resonance (EPR), mass spectra and nuclear magnetic resonance spectra. The lithographic patterns were characterized through metallurgical microscope and scanning electron microscope with a resolution at about 5 µm.

Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa. M2 macrophage polarization can reduce inflammation and repair tissue injury during AR development. Studies have substantiated the involvement of miRNAs in AR pathogenesis. Herein, the molecular mechanism of miR-214-3p in AR development was explored. To mimic the AR environment, ovalbumin (OVA) was used to treat macrophages. MiR-214-3p and glycogen synthase kinase 3 beta (GSK3B) expression in nasal mucus tissues and macrophages was assessed by RT-qPCR. The M2 phenotypic signature of CD206 in macrophages was assessed by flow cytometry. The protein expression of GSK3B and M2 macrophage markers (ARG-1 and IL-10) was evaluated by western blotting. The correlation between miR-214-3p and GSK3B was validated by a luciferase reporter assay. We found that miR-214-3p was overexpressed in macrophages and nasal mucus tissues from AR patients. MiR-214-3p facilitated M2 polarization of macrophages upon OVA stimulation. Mechanistically, miR-214-3p targeted the GSK3B 3' untranslated region in macrophages. In addition, GSK3B was downregulated in macrophages and nasal mucus tissues from AR patients. In rescue assays, GSK3B downregulation reversed the inhibitory effects of miR-214-3p silencing on M2 polarization of macrophages treated with OVA. Overall, miR-214-3p facilitates M2 macrophage polarization by targeting GSK3B.