• Chlamydia pneumoniae;
  • smooth muscle cell;
  • proliferation;
  • atherosclerosis


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.