Chlamydia pneumoniae infection of aortic smooth muscle cells reduces platelet-derived growth factor receptor-β expression

• Published in: FEMS immunology and medical microbiology 2007-11, Vol.51 (2), p.363-371
• Main Authors: Rödel, Jürgen, Lehmann, Marc, Vogelsang, Heinz, Straube, Eberhard
• Format: Article
• Language: English
• Subjects: Aorta; Arteriosclerosis; Atherogenesis; Atherosclerosis; Bacteriology; Biological and medical sciences; Cell Line; Cell Proliferation; Chlamydia; Chlamydia pneumoniae; Chlamydophila pneumoniae; Chlamydophila pneumoniae - physiology; DNA microarrays; Down-Regulation; Flow Cytometry; Fluorescence; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Profiling; Genes; Growth factors; Human behavior; Humans; Immunoblotting; Infections; Microbiology; Miscellaneous; Muscles; Myocytes, Smooth Muscle - chemistry; Myocytes, Smooth Muscle - microbiology; Oligonucleotide Array Sequence Analysis; Oligonucleotides; Pathogenesis; Plaques; Platelet-derived growth factor; Platelet-derived growth factor BB; proliferation; Protein biosynthesis; Protein synthesis; Proteins; Receptor, Platelet-Derived Growth Factor beta - biosynthesis; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA, Messenger - analysis; RNA-directed DNA polymerase; Sexually transmitted diseases; Smooth muscle; smooth muscle cell; STD; Target recognition; Transcription
• ISSN: 0928-8244; 1574-695X; 2049-632X
• DOI: 10.1111/j.1574-695X.2007.00312.x

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.