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The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells
PURPOSE: This study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARγ) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARγ agonist on the expression of PPARγ of...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Yonsei University College of Medicine
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615309/ https://www.ncbi.nlm.nih.gov/pubmed/18452259 http://dx.doi.org/10.3349/ymj.2008.49.2.230 |
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author | Kim, Yong-Hwan Choi, Si-Young Suh, Jong-Hui Kim, Tae-Kyun Seung, Ki-Bae Wang, Young-Pil Chang, Kiyuk |
author_facet | Kim, Yong-Hwan Choi, Si-Young Suh, Jong-Hui Kim, Tae-Kyun Seung, Ki-Bae Wang, Young-Pil Chang, Kiyuk |
author_sort | Kim, Yong-Hwan |
collection | PubMed |
description | PURPOSE: This study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARγ) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARγ agonist on the expression of PPARγ of C. pneumoniae-infected HCSMCs. MATERIALS AND METHODS: To determine the effect of PPARγ agonist on the proliferation of C. pneumoniae-infected HCSMCs, rosiglitazone at various concentrations was applied 1 hour before inoculation of HCSMCs. RESULTS: The expression of PPARγ mRNA in HCSMCs increased from 3 hours after C. pneumoniae infection and reached that of noninfected HCSMCs at 24 hours (p < 0.05). The expression of PPARγ protein in HCSMCs also increased from 3 hours after C. pneumoniae and persisted until 24 hours as compared with that of noninfected HCSMCs (p < 0.05). The pretreatment of HCSMCs with rosiglitazone followed by the infection with C. pneumoniae augmented the expression of PPARγ mRNA and protein (p < 0.05) and decreased cell proliferation. CONCLUSION: Our results showed that the expression of PPARγ increases in response to C. pneumoniae infection and rosiglitazone further augmented the expression of PPARγ. It is suggested that rosiglitazone could ameliorate the chronic inflammation in the vessel wall induced by C. pneumoniae by augmenting PPARγ expression. |
format | Text |
id | pubmed-2615309 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Yonsei University College of Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-26153092009-02-02 The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells Kim, Yong-Hwan Choi, Si-Young Suh, Jong-Hui Kim, Tae-Kyun Seung, Ki-Bae Wang, Young-Pil Chang, Kiyuk Yonsei Med J Original Article PURPOSE: This study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARγ) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARγ agonist on the expression of PPARγ of C. pneumoniae-infected HCSMCs. MATERIALS AND METHODS: To determine the effect of PPARγ agonist on the proliferation of C. pneumoniae-infected HCSMCs, rosiglitazone at various concentrations was applied 1 hour before inoculation of HCSMCs. RESULTS: The expression of PPARγ mRNA in HCSMCs increased from 3 hours after C. pneumoniae infection and reached that of noninfected HCSMCs at 24 hours (p < 0.05). The expression of PPARγ protein in HCSMCs also increased from 3 hours after C. pneumoniae and persisted until 24 hours as compared with that of noninfected HCSMCs (p < 0.05). The pretreatment of HCSMCs with rosiglitazone followed by the infection with C. pneumoniae augmented the expression of PPARγ mRNA and protein (p < 0.05) and decreased cell proliferation. CONCLUSION: Our results showed that the expression of PPARγ increases in response to C. pneumoniae infection and rosiglitazone further augmented the expression of PPARγ. It is suggested that rosiglitazone could ameliorate the chronic inflammation in the vessel wall induced by C. pneumoniae by augmenting PPARγ expression. Yonsei University College of Medicine 2008-04-30 2008-04-20 /pmc/articles/PMC2615309/ /pubmed/18452259 http://dx.doi.org/10.3349/ymj.2008.49.2.230 Text en Copyright © 2008 The Yonsei University College of Medicine http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Kim, Yong-Hwan Choi, Si-Young Suh, Jong-Hui Kim, Tae-Kyun Seung, Ki-Bae Wang, Young-Pil Chang, Kiyuk The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title | The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title_full | The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title_fullStr | The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title_full_unstemmed | The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title_short | The Effect of Chlamydia pneumoniae on the Expression of Peroxisome Proliferator-Activated Receptor-γ in Vascular Smooth Muscle Cells |
title_sort | effect of chlamydia pneumoniae on the expression of peroxisome proliferator-activated receptor-γ in vascular smooth muscle cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615309/ https://www.ncbi.nlm.nih.gov/pubmed/18452259 http://dx.doi.org/10.3349/ymj.2008.49.2.230 |
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