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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...

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Detalles Bibliográficos
Autores principales: Kim, Yong-Hwan, Choi, Si-Young, Suh, Jong-Hui, Kim, Tae-Kyun, Seung, Ki-Bae, Wang, Young-Pil, Chang, Kiyuk
Formato: Texto
Lenguaje:English
Publicado: Yonsei University College of Medicine 2008
Materias:
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
Descripción
Sumario: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.