Abstract
The expression of vascular adhesion molecule-1 (VCAM-1) by endothelial cells may play a major role in atherogenesis. The actual mechanisms of chlamydia pneumoniae (C. pneumoniae) relate to atherogenesis are unclear. We investigate the influence of VCAM-1 expression in the GroEL1 from C. pneumoniae-administered human coronary artery endothelial cells (HCAECs) and hypercholesterolemic rabbits. In this study, we constructed the recombinant GroEL1 from C. pneumoniae. The HCAECs/THP-1 adhesion assay, tube formation assay, western blotting, enzyme-linked immunosorbent assay, actinomycin D chase experiment, luciferase reporter assay, and immunohistochemical stainings were performed. The results show that GroEL1 increased both VCAM-1expression and THP-1 cell adhesives, and impaired tube-formation capacity in the HCAECs. GroEL1 significantly increased the VCAM-1 mRNA stability and cytosolic AU-binding factor 1 (AUF1) level. Overexpression of the p37AUF1 significantly increased VCAM-1 gene expression in GroEL1-induced bovine aortic endothelial cells (BAECs). GroEL1 prolonged the stability of VCAM-1 mRNA by increasing both p37AUF1 and the regulation of the 5′ untranslated region (UTR) of the VCAM-1 mRNA in BAECs. In hypercholesterolemic rabbits, GroEL1 administration enhanced fatty-streak and macrophage infiltration in atherosclerotic lesions, which may be mediated by elevated VCAM-1 expression. In conclusion, GroEL1 induces VCAM-1 expression by p37AUF1 in endothelial cells and enhances atherogenesis in hypercholesterolemic rabbits.
Highlights
The first known case of infection with Chlamydia pneumoniae (C. pneumoniae) was a victim of sinusitis in Taiwan
These results indicate that GroEL1 induces THP-1 cell/human coronary artery endothelial cells (HCAECs) adhesion mediated by the HCAECs’ vascular adhesion molecule-1 (VCAM-1) expression
The p37AUF1 isotype of AU-binding factor 1 (AUF1) interacts with the 59 untranslated regions (UTR) of the vascular adhesion molecule (VCAM)-1 mRNA to prolong the stability of the mRNA in GroEL1-stimulated endothelial cells
Summary
The first known case of infection with Chlamydia pneumoniae (C. pneumoniae) was a victim of sinusitis in Taiwan. Fatty streaks show C. pneumoniae accumulation and that an increase in vascular intima-media thickness is associated with C. pneumoniae seropositivity [2]. During the infectious process of C. pneumoniae, elementary bodies (EBs) require both attachment to and phagocytosis by host cells [4]. Heat shock protein 60 from C. pneumoniae ( known as GroEL1) is expressed on the surface of EBs and is the major binding protein of C. pneumoniae. GroEL1 can detach from the EBs and play an important role in the pathogenesis of infectious diseases [5]. GroEL1 causes respiratory tract and vascular diseases [6]. We have demonstrated that GroEL1 may increase the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression and accelerate atherogenesis in rabbits on a high-cholesterol diet [10]
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