Impact of Nanoparticles as an Air Pollutant on Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor in Asthma
Background: The tricellular tight junction protein angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is linked to numerous signal transduction pathways that govern gene expression, epithelial cell function, and morphogenesis. The effect of titanium dioxide (TiO<sub>2</sub>) on LS...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2024-12-01
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| Series: | Atmosphere |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2073-4433/15/12/1532 |
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| Summary: | Background: The tricellular tight junction protein angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is linked to numerous signal transduction pathways that govern gene expression, epithelial cell function, and morphogenesis. The effect of titanium dioxide (TiO<sub>2</sub>) on LSR and asthma remains unknown. The objective of the present study was to evaluate the impact of TiO<sub>2</sub> on LSR expression in asthma. Methods: A TiO<sub>2</sub>-induced animal model of asthma was established using BALB/c mice and cell lines using normal human bronchial epithelial (NHBE) lung cells and we examined LSR, RAGE, and TGFβ expression using this model. Additionally, we analyzed plasma-LSR concentrations and their correlation with clinical variables in asthma patients and control subjects. Results: The LSR concentrations in patients with asthma were lower compared to controls, and were correlated with lung function and inflammatory cell ratio. In NHBE cells treated with <i>Derp1</i>, LSR protein expression was reduced and changed by exposure to TiO<sub>2</sub>, whereas TGFβ expression was increased and changed. In mouse lungs, LSR expression was significantly reduced in OVA mice and changed in OVA/TiO<sub>2</sub> mice. Conclusion: Circulating LSR levels were decreased and correlated with clinical variables in patients with asthma, and they were influenced by TiO<sub>2</sub> exposure in mice, suggesting the potential involvement of LSR in asthma pathogenesis. |
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| ISSN: | 2073-4433 |