Editor: Patrik Bavoil
Chlamydia pneumoniae infection of aortic smooth muscle cells reduces platelet-derived growth factor receptor-β expression
Article first published online: 29 AUG 2007
FEMS Immunology & Medical Microbiology
Volume 51, Issue 2, pages 363–371, November 2007
How to Cite
Rödel, J., Lehmann, M., Vogelsang, H. and Straube, E. (2007), Chlamydia pneumoniae infection of aortic smooth muscle cells reduces platelet-derived growth factor receptor-β expression. FEMS Immunology & Medical Microbiology, 51: 363–371. doi: 10.1111/j.1574-695X.2007.00312.x
- Issue published online: 29 AUG 2007
- Article first published online: 29 AUG 2007
- Received 10 April 2007; revised 10 July 2007; accepted 10 July 2007.First published online October 2007.
- Chlamydia pneumoniae;
- smooth muscle cell;
Chlamydia pneumoniae infection may play a role in the pathogenesis of atherosclerosis. In this study, an oligonucleotide microarray was utilized to examine the transcriptional response of human aortic smooth muscle cells (AoSMC) to C. pneumoniae infection. Alteration of mRNA expression in 71 out of 780 genes was detected at 24 h after infection. Among the down-regulated genes, platelet-derived growth factor receptor-β (PDGFR-β) was identified as a target for further analysis because the PDGF system is involved in the fibroproliferative response of SMC in atherogenesis. Reverse transcriptase PCR analysis demonstrated that C. pneumoniae inhibits the up-regulation of PDGFR-β mRNA occurring in AoSMC after mock infection. PDGFR-β protein synthesis was examined by immunoblotting and fluorescence-activated cell sorting. Compared with mock-infected cells, the amount of receptor protein was reduced at 24, 48, and 72 h after infection. Diminished PDGFR-β synthesis in infected cultures was accompanied by the suppression of AoSMC growth following PDGF-BB stimulation. The interference of C. pneumoniae with PDGFR-β expression may result in decreased SMC proliferation in atherosclerotic plaques, thereby affecting the development and stability of advanced lesions.