GroEL1, from chlamydia pneumoniae, induces vascular adhesion molecule 1 expression by p37AUF1 in endothelial cells and hypercholesterolemic rabbit

Chun Yao Huang, Chun Ming Shih, Nai Wen Tsao, Yung Hsiang Chen, Chi Yuan Li, Yu Jia Chang, Nen Chung Chang, Keng Liang Ou, Cheng Yen Lin, Yi Wen Lin, Chih Hao Nien, Feng Yen Lin

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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.

Original languageEnglish
Article numbere42808
JournalPLoS One
Volume7
Issue number8
DOIs
Publication statusPublished - Aug 10 2012

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Chlamydophila pneumoniae
Endothelial cells
blood vessels
endothelial cells
Blood Vessels
adhesion
Adhesion
Endothelial Cells
rabbits
Rabbits
Molecules
atherogenesis
Assays
coronary vessels
Atherosclerosis
Coronary Vessels
Messenger RNA
assays
5' Untranslated Regions
Immunosorbents

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

GroEL1, from chlamydia pneumoniae, induces vascular adhesion molecule 1 expression by p37AUF1 in endothelial cells and hypercholesterolemic rabbit. / Huang, Chun Yao; Shih, Chun Ming; Tsao, Nai Wen; Chen, Yung Hsiang; Li, Chi Yuan; Chang, Yu Jia; Chang, Nen Chung; Ou, Keng Liang; Lin, Cheng Yen; Lin, Yi Wen; Nien, Chih Hao; Lin, Feng Yen.

In: PLoS One, Vol. 7, No. 8, e42808, 10.08.2012.

Research output: Contribution to journalArticle

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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.",
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AU - Huang, Chun Yao

AU - Shih, Chun Ming

AU - Tsao, Nai Wen

AU - Chen, Yung Hsiang

AU - Li, Chi Yuan

AU - Chang, Yu Jia

AU - Chang, Nen Chung

AU - Ou, Keng Liang

AU - Lin, Cheng Yen

AU - Lin, Yi Wen

AU - Nien, Chih Hao

AU - Lin, Feng Yen

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N2 - 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.

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