Affiliation:
1. Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China
Abstract
ABSTRACT
The migration of vascular smooth muscle cells (VSMCs) from the media to the intima is proposed to be a key event in the development of atherosclerosis. Recently, we reported that
Chlamydia pneumoniae
infection is involved in VSMC migration. However, the exact mechanisms for
C. pneumoniae
infection-induced VSMC migration are not yet well elucidated. In this study, we examined the role of the Toll-like receptor 2 (TLR2) activation-related signaling pathway in VSMC migration induced by
C. pneumoniae
infection. An Affymetrix-based gene expression array was conducted to identify the changes of gene expression in rat primary VSMCs (rVSMCs) infected with
C. pneumoniae
. Both the microarray analysis and quantitative real-time reverse transcription (RT)-PCR revealed that TLR2 mRNA expression was strongly upregulated 12 h after
C. pneumoniae
infection. RT-PCR and Western blot analysis further showed that the expression levels of TLR2 mRNA and protein significantly increased at the different time points after infection. Immunocytochemical analysis suggested a TLR2 recruitment to the vicinity of
C. pneumoniae
inclusions. Cell migration assays showed that the TLR2-neutralizing antibody could significantly inhibit
C. pneumoniae
infection-induced rVSMC migration. In addition,
C. pneumoniae
infection stimulated Akt phosphorylation at Ser 473, which was obviously suppressed by the PI3K inhibitor LY294002, thereby inhibiting rVSMC migration caused by
C. pneumoniae
infection. Furthermore, both the infection-induced Akt phosphorylation and rVSMC migration were suppressed by the TLR2-neutralizing antibody. Taken together, these data suggest that
C. pneumoniae
infection can promote VSMC migration possibly through the TLR2-related signaling pathway.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
19 articles.
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