Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.

Tracheal stenosis is a refractory and recurrent disease induced by excessive cell proliferation within the restricted tracheal space. We investigated the role of extracellular signal-regulated kinase (ERK), which mediates a broad range of intracellular signal transduction processes in tracheal steno...

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Autores principales:	Akari Kimura, Koji Araki, Yasushi Satoh, Sachiyo Mogi, Kazuko Fujitani, Takaomi Kurioka, Shogo Endo, Akihiro Shiotani, Taku Yamashita
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b4fc6ab9f6cc4ed390cfdc81d7d1c287
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spelling	oai:doaj.org-article:b4fc6ab9f6cc4ed390cfdc81d7d1c2872021-12-02T20:07:58ZInhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.1932-620310.1371/journal.pone.0256127https://doaj.org/article/b4fc6ab9f6cc4ed390cfdc81d7d1c2872021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0256127https://doaj.org/toc/1932-6203Tracheal stenosis is a refractory and recurrent disease induced by excessive cell proliferation within the restricted tracheal space. We investigated the role of extracellular signal-regulated kinase (ERK), which mediates a broad range of intracellular signal transduction processes in tracheal stenosis and the therapeutic effect of the MEK inhibitor which is the upstream kinase of ERK. We histologically analyzed cauterized tracheas to evaluate stenosis using a tracheal stenosis mouse model. Using Western blot, we analyzed the phosphorylation rate of ERK1/2 after cauterization with or without MEK inhibitor. MEK inhibitor was intraperitoneally injected 30 min prior to cauterization (single treatment) or 30 min prior to and 24, 48, 72, and 96 hours after cauterization (daily treatment). We compared the stenosis of non-inhibitor treatment, single treatment, and daily treatment group. We successfully established a novel mouse model of tracheal stenosis. The cauterized trachea increased the rate of stenosis compared with the normal control trachea. The phosphorylation rate of ERK1 and ERK2 was significantly increased at 5 min after the cauterization compared with the normal controls. After 5 min, the rates decreased over time. The daily treatment group had suppressed stenosis compared with the non-inhibitor treatment group. p-ERK1/2 activation after cauterization could play an important role in the tracheal wound healing process. Consecutive inhibition of ERK phosphorylation is a potentially useful therapeutic strategy for tracheal stenosis.Akari KimuraKoji ArakiYasushi SatohSachiyo MogiKazuko FujitaniTakaomi KuriokaShogo EndoAkihiro ShiotaniTaku YamashitaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 9, p e0256127 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Akari Kimura Koji Araki Yasushi Satoh Sachiyo Mogi Kazuko Fujitani Takaomi Kurioka Shogo Endo Akihiro Shiotani Taku Yamashita Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
description	Tracheal stenosis is a refractory and recurrent disease induced by excessive cell proliferation within the restricted tracheal space. We investigated the role of extracellular signal-regulated kinase (ERK), which mediates a broad range of intracellular signal transduction processes in tracheal stenosis and the therapeutic effect of the MEK inhibitor which is the upstream kinase of ERK. We histologically analyzed cauterized tracheas to evaluate stenosis using a tracheal stenosis mouse model. Using Western blot, we analyzed the phosphorylation rate of ERK1/2 after cauterization with or without MEK inhibitor. MEK inhibitor was intraperitoneally injected 30 min prior to cauterization (single treatment) or 30 min prior to and 24, 48, 72, and 96 hours after cauterization (daily treatment). We compared the stenosis of non-inhibitor treatment, single treatment, and daily treatment group. We successfully established a novel mouse model of tracheal stenosis. The cauterized trachea increased the rate of stenosis compared with the normal control trachea. The phosphorylation rate of ERK1 and ERK2 was significantly increased at 5 min after the cauterization compared with the normal controls. After 5 min, the rates decreased over time. The daily treatment group had suppressed stenosis compared with the non-inhibitor treatment group. p-ERK1/2 activation after cauterization could play an important role in the tracheal wound healing process. Consecutive inhibition of ERK phosphorylation is a potentially useful therapeutic strategy for tracheal stenosis.
format	article
author	Akari Kimura Koji Araki Yasushi Satoh Sachiyo Mogi Kazuko Fujitani Takaomi Kurioka Shogo Endo Akihiro Shiotani Taku Yamashita
author_facet	Akari Kimura Koji Araki Yasushi Satoh Sachiyo Mogi Kazuko Fujitani Takaomi Kurioka Shogo Endo Akihiro Shiotani Taku Yamashita
author_sort	Akari Kimura
title	Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
title_short	Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
title_full	Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
title_fullStr	Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
title_full_unstemmed	Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
title_sort	inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/b4fc6ab9f6cc4ed390cfdc81d7d1c287
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Inhibition of extracellular signal-regulated kinase pathway suppresses tracheal stenosis in a novel mouse model.

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