Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.

The proliferation, differentiation, and migration of keratinocytes are essential in the early stages of wound healing. Hypoxia-Reoxygenation (H/R) injury to keratinocytes can occur in various stressful environments such as surgery, trauma, and various forms of ulcers. The effects of remifentanil on...

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Main Authors: Jae-Young Kwon, Bong-Soo Park, Yong-Ho Kim, Yong-Deok Kim, Cheul-Hong Kim, Ji-Young Yoon, Ji-Uk Yoon
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4304791?pdf=render
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author Jae-Young Kwon
Bong-Soo Park
Yong-Ho Kim
Yong-Deok Kim
Cheul-Hong Kim
Ji-Young Yoon
Ji-Uk Yoon
author_facet Jae-Young Kwon
Bong-Soo Park
Yong-Ho Kim
Yong-Deok Kim
Cheul-Hong Kim
Ji-Young Yoon
Ji-Uk Yoon
author_sort Jae-Young Kwon
collection DOAJ
description The proliferation, differentiation, and migration of keratinocytes are essential in the early stages of wound healing. Hypoxia-Reoxygenation (H/R) injury to keratinocytes can occur in various stressful environments such as surgery, trauma, and various forms of ulcers. The effects of remifentanil on human keratinocytes under hypoxia-reoxygenation have not been fully studied. Therefore, we investigated the effects of remifentanil on the proliferation, apoptosis, and autophagic activation of human keratinocytes during hypoxic-reoxygenation. Human keratinocytes were cultured under 1% oxygen tension for 24 h. The cells were then treated with various concentrations of remifentanil (0.01, 0.1, 0.5, and 1 ng/mL) for 2 h. Thereafter, the cells were reoxygenated for 12 h at 37°C. We measured cell viability via MTT assay. Using quantitative real-time PCR and western blot analysis, we measured the expression levels of proteins associated with apoptosis and autophagy. Quantification of apoptotic cells was performed using flow cytometer analysis and autophagic vacuoles were observed under a fluorescence microscope. Remifentanil treatment brought about an increase in the proliferation of human keratinocytes damaged by hypoxia-reoxygenation and decreased the apoptotic cell death, enhancing autophagic activity. However, the autophagy pathway inhibitor 3-MA inhibited the protective effect of remifentanil in hypoxia-reoxygenation injury. In conclusion, the current study demonstrated that remifentanil treatment stimulated autophagy and reduced apoptotic cell death in a hypoxia-reoxygenation model of human keratinocytes. Our results provide additional insights into the relationship between apoptosis and autophagy.
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spelling doaj.art-5f18709c5eb34b6180eea9c88578b5092022-12-22T00:40:22ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01101e011698210.1371/journal.pone.0116982Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.Jae-Young KwonBong-Soo ParkYong-Ho KimYong-Deok KimCheul-Hong KimJi-Young YoonJi-Uk YoonThe proliferation, differentiation, and migration of keratinocytes are essential in the early stages of wound healing. Hypoxia-Reoxygenation (H/R) injury to keratinocytes can occur in various stressful environments such as surgery, trauma, and various forms of ulcers. The effects of remifentanil on human keratinocytes under hypoxia-reoxygenation have not been fully studied. Therefore, we investigated the effects of remifentanil on the proliferation, apoptosis, and autophagic activation of human keratinocytes during hypoxic-reoxygenation. Human keratinocytes were cultured under 1% oxygen tension for 24 h. The cells were then treated with various concentrations of remifentanil (0.01, 0.1, 0.5, and 1 ng/mL) for 2 h. Thereafter, the cells were reoxygenated for 12 h at 37°C. We measured cell viability via MTT assay. Using quantitative real-time PCR and western blot analysis, we measured the expression levels of proteins associated with apoptosis and autophagy. Quantification of apoptotic cells was performed using flow cytometer analysis and autophagic vacuoles were observed under a fluorescence microscope. Remifentanil treatment brought about an increase in the proliferation of human keratinocytes damaged by hypoxia-reoxygenation and decreased the apoptotic cell death, enhancing autophagic activity. However, the autophagy pathway inhibitor 3-MA inhibited the protective effect of remifentanil in hypoxia-reoxygenation injury. In conclusion, the current study demonstrated that remifentanil treatment stimulated autophagy and reduced apoptotic cell death in a hypoxia-reoxygenation model of human keratinocytes. Our results provide additional insights into the relationship between apoptosis and autophagy.http://europepmc.org/articles/PMC4304791?pdf=render
spellingShingle Jae-Young Kwon
Bong-Soo Park
Yong-Ho Kim
Yong-Deok Kim
Cheul-Hong Kim
Ji-Young Yoon
Ji-Uk Yoon
Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
PLoS ONE
title Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
title_full Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
title_fullStr Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
title_full_unstemmed Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
title_short Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.
title_sort remifentanil protects human keratinocytes against hypoxia reoxygenation injury through activation of autophagy
url http://europepmc.org/articles/PMC4304791?pdf=render
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