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Int. J. Mol. Sci. 2017, 18(5), 920; doi:10.3390/ijms18050920

YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

1
School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan
2
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
3
Division of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung 40402, Taiwan
4
Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan
5
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 40402, Taiwan
6
School of Medicine, China Medical University, Taichung 40402, Taiwan
7
Department of Medicine, Mackay Medical College, New Taipei City 25160, Taiwan
8
Department of Biotechnology, College of Health Science, Asia University, Taichung 40402, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editor: Joseph V. Moxon
Received: 5 March 2017 / Revised: 19 April 2017 / Accepted: 21 April 2017 / Published: 27 April 2017
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
View Full-Text   |   Download PDF [4666 KB, uploaded 27 April 2017]   |  

Abstract

YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis. View Full-Text
Keywords: YKL-40; IL-18; osteoblasts; angiogenesis; rheumatoid arthritis YKL-40; IL-18; osteoblasts; angiogenesis; rheumatoid arthritis
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MDPI and ACS Style

Li, T.-M.; Liu, S.-C.; Huang, Y.-H.; Huang, C.-C.; Hsu, C.-J.; Tsai, C.-H.; Wang, S.-W.; Tang, C.-H. YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells. Int. J. Mol. Sci. 2017, 18, 920.

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