Modulation of TNF-α-induced endothelial cell activation by glucosamine, a naturally occurring amino monosaccharide

Ju,Yinghua; Hua,Jian; Sakamoto,Koji; Ogawa,Hideoki; Nagaoka,Isao

doi:10.3892/ijmm_00000089

December 2008 Volume 22 Issue 6

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December 2008 Volume 22 Issue 6

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Article

Modulation of TNF-α-induced endothelial cell activation by glucosamine, a naturally occurring amino monosaccharide

Authors:
- Yinghua Ju
- Jian Hua
- Koji Sakamoto
- Hideoki Ogawa
- Isao Nagaoka
View Affiliations / Copyright

Affiliations: Department of Host Defense and Biochemical Research, Juntendo University, School of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421
Pages: 809-815
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Published online on: December 1, 2008

https://doi.org/10.3892/ijmm_00000089
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Abstract

Atherosclerosis is now considered a chronic inflammatory disease, and glucosamine has the potential to exhibit an anti-inflammatory action. Thus, we investigated the effect of glucosamine on tumor necrosis factor α (TNF-α)-induced endothelial cell activation. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNF-α in the presence or absence of glucosamine or its analogue, N-acetylglucosamine. mRNA expression of MCP-1 (a chemoattractant protein) and ICAM-1 (an adhesion molecule) was evaluated by real-time RT-PCR, and their protein levels were analyzed by ELISA and Western blotting, respectively. Furthermore, the effects of glucosamine on the phosphorylation of p38MAPK and NF-κB, and O-N-acetylglucosamine (O-GlcNAc) modification were evaluated by Western blotting. The results demonstrated that glucosamine but not N-acetylglucosamine suppressed TNF-α-induced expression of MCP-1 and ICAM-1 at both the mRNA and protein levels. Furthermore, glucosamine abrogated the phosphorylation of p38MAPK and NF-κB. To note, glucosamine induced O-GlcNAc modification, which was negatively correlated with the expression of MCP-1 and ICAM-1, and phosphorylation of p38MAPK and NF-κB. Thus, glucosamine is likely to suppress endothelial cell activation (TNF-α-induced ICAM-1 and MCP-1 expression) possibly by affecting p38MAPK and NF-κB signaling via O-GlcNAc modification.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Modulation of TNF-α-induced endothelial cell activation by glucosamine, a naturally occurring amino monosaccharide

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