Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways

Tao Cheng Wu; Chih Yao Chiang; Jenq Shyong Chan; Chiu Yang Lee; Hsin Bang Leu; Po Hsun Huang; Jia Shiong Chen; Shing Jong Lin; Jaw Wen Chen

doi:10.1089/jir.2018.0009

Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways

Tao Cheng Wu, Chih Yao Chiang, Jenq Shyong Chan, Chiu Yang Lee, Hsin Bang Leu, Po Hsun Huang, Jia Shiong Chen, Shing Jong Lin, Jaw Wen Chen

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

Rheumatoid arthritis (RA) with diabetes increases the risk of cardiovascular diseases. Interleukin-6 (IL-6) promotes the disease activity of RA and insulin resistance. This study aimed to evaluate the potential effects and molecular mechanisms of IL-6 blocker, tocilizumab, in atherosclerosis with diabetes. Human aortic smooth muscle cells (HASMCs) cultured under hyperglycemic conditions were evaluated for migration, expression of adhesion molecules, and matrix metalloproteinases before and after treatment with tocilizumab. High glucose (HG) significantly increased expression of IL-6, intercellular adhesion molecule (ICAM-1), matrix metalloproteinase-2 & 9, and migration of vascular smooth muscle cells. Tocilizumab suppressed HG-induced expression of ICAM-1, MMP-2, and MMP-9. Pretreatment with tocilizumab also inhibited migration, MAPK signaling, and nuclear translocation of p65-NF-κB in HG-stimulated HASMCs. Our data suggested that tocilizumab may exert an antiatherosclerotic activity in diabetes.

Original language	English
Pages (from-to)	510-516
Number of pages	7
Journal	Journal of Interferon and Cytokine Research
Volume	38
Issue number	11
DOIs	https://doi.org/10.1089/jir.2018.0009
Publication status	Published - Nov 2018
Externally published	Yes

Keywords

diabetes
glucose
human aortic smooth muscle cells
interleukin-6 receptor
tocilizumab

ASJC Scopus subject areas

Immunology
Cell Biology
Virology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1089/jir.2018.0009

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Wu, T. C., Chiang, C. Y., Chan, J. S., Lee, C. Y., Leu, H. B., Huang, P. H., Chen, J. S., Lin, S. J., & Chen, J. W. (2018). Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways. Journal of Interferon and Cytokine Research, 38(11), 510-516. https://doi.org/10.1089/jir.2018.0009

Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways. / Wu, Tao Cheng; Chiang, Chih Yao; Chan, Jenq Shyong et al.
In: Journal of Interferon and Cytokine Research, Vol. 38, No. 11, 11.2018, p. 510-516.

Research output: Contribution to journal › Article › peer-review

Wu, TC, Chiang, CY, Chan, JS, Lee, CY, Leu, HB, Huang, PH, Chen, JS, Lin, SJ & Chen, JW 2018, 'Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways', Journal of Interferon and Cytokine Research, vol. 38, no. 11, pp. 510-516. https://doi.org/10.1089/jir.2018.0009

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abstract = "Rheumatoid arthritis (RA) with diabetes increases the risk of cardiovascular diseases. Interleukin-6 (IL-6) promotes the disease activity of RA and insulin resistance. This study aimed to evaluate the potential effects and molecular mechanisms of IL-6 blocker, tocilizumab, in atherosclerosis with diabetes. Human aortic smooth muscle cells (HASMCs) cultured under hyperglycemic conditions were evaluated for migration, expression of adhesion molecules, and matrix metalloproteinases before and after treatment with tocilizumab. High glucose (HG) significantly increased expression of IL-6, intercellular adhesion molecule (ICAM-1), matrix metalloproteinase-2 & 9, and migration of vascular smooth muscle cells. Tocilizumab suppressed HG-induced expression of ICAM-1, MMP-2, and MMP-9. Pretreatment with tocilizumab also inhibited migration, MAPK signaling, and nuclear translocation of p65-NF-κB in HG-stimulated HASMCs. Our data suggested that tocilizumab may exert an antiatherosclerotic activity in diabetes.",

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AB - Rheumatoid arthritis (RA) with diabetes increases the risk of cardiovascular diseases. Interleukin-6 (IL-6) promotes the disease activity of RA and insulin resistance. This study aimed to evaluate the potential effects and molecular mechanisms of IL-6 blocker, tocilizumab, in atherosclerosis with diabetes. Human aortic smooth muscle cells (HASMCs) cultured under hyperglycemic conditions were evaluated for migration, expression of adhesion molecules, and matrix metalloproteinases before and after treatment with tocilizumab. High glucose (HG) significantly increased expression of IL-6, intercellular adhesion molecule (ICAM-1), matrix metalloproteinase-2 & 9, and migration of vascular smooth muscle cells. Tocilizumab suppressed HG-induced expression of ICAM-1, MMP-2, and MMP-9. Pretreatment with tocilizumab also inhibited migration, MAPK signaling, and nuclear translocation of p65-NF-κB in HG-stimulated HASMCs. Our data suggested that tocilizumab may exert an antiatherosclerotic activity in diabetes.

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Tocilizumab, a humanized monoclonal antibody against the interleukin-6 receptor, inhibits high glucose-induced vascular smooth muscle cell migration through mitogen-activated protein kinase signaling pathways

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

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