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Atherosclerosis. 2014 Aug;235(2):519-25. doi: 10.1016/j.atherosclerosis.2014.05.943. Epub 2014 Jun 9.

Chlamydia pneumoniae negatively regulates ABCA1 expression via TLR2-Nuclear factor-kappa B and miR-33 pathways in THP-1 macrophage-derived foam cells.

Author information

1
Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang 421001, China; Department of Histology and Embryology, Guilin Medical University, Guilin, Guangxi 541004, China.
2
Department of Histology and Embryology, University of South China, Hengyang, Hunan 421001, China.
3
Department of Intensive Care Unit, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, China.
4
Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang 421001, China.
5
Second Affiliated Hospital of University of South China, Hengyang, Hunan 421001, China.
6
Fourth Year Student in Department of Biochemistry, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
7
Department of Biochemistry and Molecular Biology, The Libin Cardiovascular Institute of Alberta, The University of Calgary, Health Sciences Center, 3330 Hospital Dr NW, Calgary, Alberta T2N 4N1, Canada.
8
Second Affiliated Hospital of University of South China, Hengyang, Hunan 421001, China. Electronic address: tianguopingnhfe@163.com.
9
Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang 421001, China. Electronic address: tangchaoke@qq.com.

Abstract

OBJECTIVES:

ATP-binding cassette transporter A1 (ABCA1) is critical in exporting cholesterol from macrophages and plays a protective role in the development of atherosclerosis. This study was to determine the effects and potential mechanisms of Chlamydia pneumoniae (C. pneumoniae) on ABCA1 expression and cellular cholesterol efflux in THP-1 macrophage-derived foam cells.

METHODS AND RESULTS:

C. pneumoniae significantly decreased the expression of ABCA1 and reduced cholesterol efflux. Furthermore, we found that C. pneumoniae suppressed ABCA1 expression via up-regulation of miR-33s. The inhibition of C. pneumoniae-induced NF-κB activation decreased miR-33s expression and enhanced ABCA1 expression. In addition, C. pneumoniae increased Toll-like receptor 2 (TLR2) expressions, inhibition of which by siRNA could also block NF-κB activation and miR-33s expression, and promot the expression of ABCA1.

CONCLUSION:

Taken together, these results reveal that C. pneumoniae may negatively regulate ABCA1 expression via TLR2-NF-κB and miR-33 pathways in THP-1 macrophage-derived foam cells, which may provide new insights for understanding the effects of C. pneumoniae on the pathogenesis of atherosclerosis.

KEYWORDS:

ABCA1; Atherosclerosis; Chlamydia pneumoniae; NF-κB; TLR2; miR-33s

[Indexed for MEDLINE]

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