Induced expression of lectin-like oxidized ldl receptor-1 in vascular smooth muscle cells following Chlamydia pneumoniae infection and its down-regulation by fluvastatin

Prochnau, D. and Rödel, J. and Prager, Katrin and Kuersten, Dana and Heller, Regine and Straube, E. and Figulla, H. R. (2010) Induced expression of lectin-like oxidized ldl receptor-1 in vascular smooth muscle cells following Chlamydia pneumoniae infection and its down-regulation by fluvastatin. Acta Microbiologica et Immunologica Hungarica, 57 (2). pp. 147-155. ISSN 1217-8950

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Abstract

Microorganisms such as Chlamydia pneumoniae have been shown to infect vascular cells and are believed to contribute to vascular inflammation and atherosclerotic plaque development. Plasma levels of oxidized low density lipoprotein (oxLDL) have received considerable attention as potential predictors of prognosis in atherosclerotic diseases. Lectin-like oxidized LDL receptor-1 (LOX-1) is one of the major receptors for oxidized LDL. It was investigated whether C. pneumoniae infection can stimulate expression of LOX-1 in vascular smooth muscle cells. Expression of LOX-1 in VSMC was measured by RT-PCR and immunoblotting following C. pneumoniae infection. To examine the pharmacological effect of a HMG-CoA reductase inhibitor on LOX-1 expression, cells were co-incubated with fluvastatin immediately after infection. Adose and time dependent expression of LOX-1mRNAand protein was found in C. pneumoniae infected SMC. After heat and UV light treatment of the chlamydial inoculum the level of LOX-1 was reduced to that of mock-infected cultures. Furthermore, treatment of infected cells with fluvastatin decreased LOX-1 expression to baseline levels. The up-regulation of LOX-1 induced by C. pneumoniae could lead to continued lipid accumulation in atherosclerotic lesions. Together with the widespread expression of LOX-1, this might contribute to the epidemiologic link between C. pneumoniae infection and atherosclerosis. The effect of lowering the LOX-1 expression by fluvastatin may provide a pharmacological option of limiting oxLDL uptake via its scavenger receptor.

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