ArticleYonsei medical journal2008
The effect of Chlamydia pneumoniae on the expression of peroxisome proliferator-activated receptor-gamma in vascular smooth muscle cells.
Article in Yonsei medical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 4 citations in OpenAlex.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARgamma) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARgamma agonist on the expression of PPARgamma of C. pneumoniae-infected HCSMCs. MATERIALS AND
methodsTo determine the effect of PPARgamma agonist on the proliferation of C. pneumoniae-infected HCSMCs, rosiglitazone at various concentrations was applied 1 hour before inoculation of HCSMCs.
resultsThe expression of PPARgamma 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 PPARgamma 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 PPARgamma mRNA and protein (p<0.05) and decreased cell proliferation.
conclusionOur results showed that the expression of PPARgamma increases in response to C. pneumoniae infection and rosiglitazone further augmented the expression of PPARgamma. It is suggested that rosiglitazone could ameliorate the chronic inflammation in the vessel wall induced by C. pneumoniae by augmenting PPARgamma expression.
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