Version 1
: Received: 25 April 2023 / Approved: 28 April 2023 / Online: 28 April 2023 (11:07:00 CEST)
Version 2
: Received: 24 May 2023 / Approved: 25 May 2023 / Online: 25 May 2023 (09:30:03 CEST)
How to cite:
Hwang, D.Y.; An, M.; Lee, P.; Kim, J.; Nam, Y.; Park, S.; Baek, A.; Jang, A. Particulate Matter as One of Air Pollutants Impacts Asthma via the Tricellular Tight Junction Protein, LSR. Preprints2023, 2023041171. https://doi.org/10.20944/preprints202304.1171.v2
Hwang, D.Y.; An, M.; Lee, P.; Kim, J.; Nam, Y.; Park, S.; Baek, A.; Jang, A. Particulate Matter as One of Air Pollutants Impacts Asthma via the Tricellular Tight Junction Protein, LSR. Preprints 2023, 2023041171. https://doi.org/10.20944/preprints202304.1171.v2
Hwang, D.Y.; An, M.; Lee, P.; Kim, J.; Nam, Y.; Park, S.; Baek, A.; Jang, A. Particulate Matter as One of Air Pollutants Impacts Asthma via the Tricellular Tight Junction Protein, LSR. Preprints2023, 2023041171. https://doi.org/10.20944/preprints202304.1171.v2
APA Style
Hwang, D.Y., An, M., Lee, P., Kim, J., Nam, Y., Park, S., Baek, A., & Jang, A. (2023). Particulate Matter as One of Air Pollutants Impacts Asthma via the Tricellular Tight Junction Protein, LSR. Preprints. https://doi.org/10.20944/preprints202304.1171.v2
Chicago/Turabian Style
Hwang, D.Y., Ae-Rin Baek and An-Soo Jang. 2023 "Particulate Matter as One of Air Pollutants Impacts Asthma via the Tricellular Tight Junction Protein, LSR" Preprints. https://doi.org/10.20944/preprints202304.1171.v2
Abstract
The tricellular tight junction protein angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is associated with numerous signal transduction pathways that regulate gene expression, epithelial cell function, and morphogenesis. The impacts of particulate matter on LSR and asthma are not known. Therefore, the aim of the present study was to assess the impacts of particulate matter as one of air pollution on LSR expression in asthma. To this end, we investigated the involvement of LSR in the pathogenesis of bronchial asthma in an ovalbumin (OVA) mouse model of asthma exposed to titanium dioxide (TiO2), and examined plasma LSR levels and their relationship with clinical variables in asthma patients and healthy controls. Plasma LSR levels were lower in asthma patients than in healthy controls. Although plasma levels of receptor for advanced glycation end-products (RAGE) were lower in asthma patients than in healthy controls, high mobility group box protein 1 (HMGB1) levels did not differ between these groups. In asthma patients, LSR levels were correlated with the forced vital capacity percentage, ratio of forced expiration (first second)-to-forced vital capacity, white blood cell count, and blood lymphocyte proportion. In mice, LSR expression was significantly decreased in OVA mice compared with control mice, and changed in OVA mice exposed to TiO2. Transforming growth factor beta levels were increased in OVA mice compared with control mice, and changed in OVA mice exposed to TiO2. Overall, plasma LSR levels were decreased in asthma patients, and were influenced by exposure to air pollution. These findings suggest the involvement of LSR in the pathogenesis of asthma.
Biology and Life Sciences, Immunology and Microbiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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