Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice
Purpose Inhalation of air containing high amounts of particular matter (PM) causes various respiratory disorders including asthma, chronic obstructive pulmonary disease, and lung cancer. The changes of expression of inflammatory factors by polydeoxyribonucleotide (PDRN) administration in the PM10-ex...
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Korean Continence Society
2021-05-01
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doaj-cd99faa6a77541d197ee962edf4375a62021-05-31T04:30:55ZengKorean Continence SocietyInternational Neurourology Journal2093-47772093-69312021-05-0125Suppl 1S192610.5213/inj.2142168.084950Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed MiceLakkyong Hwang0Jun-Jang Jin1Il-Gyu Ko2Suyeon Kim3Young-A Cho4Jun-Seok Sung5Cheon Woong Choi6Bok Soon Chang7 Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea Department of Medicine, Graduate School, Kyung Hee University, Seoul, Korea Department of Medicine, Graduate School, Kyung Hee University, Seoul, Korea Department of Medicine, Graduate School, Kyung Hee University, Seoul, Korea Department of Pulmonary, Allergy and Critical Care Medicine, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea Department of Pulmonary, Allergy and Critical Care Medicine, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, KoreaPurpose Inhalation of air containing high amounts of particular matter (PM) causes various respiratory disorders including asthma, chronic obstructive pulmonary disease, and lung cancer. The changes of expression of inflammatory factors by polydeoxyribonucleotide (PDRN) administration in the PM10-exposed trachea inflammation model were evaluated. Methods PM10 was administered to mouse trachea to induce acute inflammatory damage, and changes in inflammatory factors were observed after administration of PDRN and 3,7-dimethyl-1-propargylxanthine (DMPX) for 3 days daily. Expression of inflammatory cytokines, adenosine A2A receptor (A2AR), protein kinase A (PKA), 3΄,5΄-cyclic adenosine monophosphate responsive element binding protein (CREB) were detected by enzyme‐linked immunosorbent assay, immunofluorescence, and western blot assay. Results PM-exposed trachea showed increased tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression, and expression of TNF-α and IL-1β was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased nuclear factor (NF)-κB phosphorylation, and phosphorylation of nuclear factor-kappa B was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased expression of A2AR, but PDRN treatment more enhanced A2AR expression in PM-exposed mice. PKA phosphorylation was not changed and CREP phosphorylation was decreased, however PDRN treatment increased phosphorylation of PKA and CREB in PM-exposed mice. DMPX treatment blocked all the effects of PDRN on PM-exposed mice, demonstrating that the action of PDRN occurs via A2AR. Conclusions PDRN treatment attenuated inflammation in the trachea of the PM10-exposed mice. This improving effect of PDRN can be ascribed to the activation of A2AR through the cAMP-PKA pathway.http://www.einj.org/upload/pdf/inj-2142168-084.pdfparticulate matterpolydeoxyribonucleotideadenosine a2a receptorinflammation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lakkyong Hwang Jun-Jang Jin Il-Gyu Ko Suyeon Kim Young-A Cho Jun-Seok Sung Cheon Woong Choi Bok Soon Chang |
spellingShingle |
Lakkyong Hwang Jun-Jang Jin Il-Gyu Ko Suyeon Kim Young-A Cho Jun-Seok Sung Cheon Woong Choi Bok Soon Chang Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice International Neurourology Journal particulate matter polydeoxyribonucleotide adenosine a2a receptor inflammation |
author_facet |
Lakkyong Hwang Jun-Jang Jin Il-Gyu Ko Suyeon Kim Young-A Cho Jun-Seok Sung Cheon Woong Choi Bok Soon Chang |
author_sort |
Lakkyong Hwang |
title |
Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice |
title_short |
Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice |
title_full |
Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice |
title_fullStr |
Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice |
title_full_unstemmed |
Polydeoxyribonucleotide Attenuates Airway Inflammation Through AR Signaling Pathway in PM-Exposed Mice |
title_sort |
polydeoxyribonucleotide attenuates airway inflammation through ar signaling pathway in pm-exposed mice |
publisher |
Korean Continence Society |
series |
International Neurourology Journal |
issn |
2093-4777 2093-6931 |
publishDate |
2021-05-01 |
description |
Purpose Inhalation of air containing high amounts of particular matter (PM) causes various respiratory disorders including asthma, chronic obstructive pulmonary disease, and lung cancer. The changes of expression of inflammatory factors by polydeoxyribonucleotide (PDRN) administration in the PM10-exposed trachea inflammation model were evaluated. Methods PM10 was administered to mouse trachea to induce acute inflammatory damage, and changes in inflammatory factors were observed after administration of PDRN and 3,7-dimethyl-1-propargylxanthine (DMPX) for 3 days daily. Expression of inflammatory cytokines, adenosine A2A receptor (A2AR), protein kinase A (PKA), 3΄,5΄-cyclic adenosine monophosphate responsive element binding protein (CREB) were detected by enzyme‐linked immunosorbent assay, immunofluorescence, and western blot assay. Results PM-exposed trachea showed increased tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression, and expression of TNF-α and IL-1β was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased nuclear factor (NF)-κB phosphorylation, and phosphorylation of nuclear factor-kappa B was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased expression of A2AR, but PDRN treatment more enhanced A2AR expression in PM-exposed mice. PKA phosphorylation was not changed and CREP phosphorylation was decreased, however PDRN treatment increased phosphorylation of PKA and CREB in PM-exposed mice. DMPX treatment blocked all the effects of PDRN on PM-exposed mice, demonstrating that the action of PDRN occurs via A2AR. Conclusions PDRN treatment attenuated inflammation in the trachea of the PM10-exposed mice. This improving effect of PDRN can be ascribed to the activation of A2AR through the cAMP-PKA pathway. |
topic |
particulate matter polydeoxyribonucleotide adenosine a2a receptor inflammation |
url |
http://www.einj.org/upload/pdf/inj-2142168-084.pdf |
work_keys_str_mv |
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