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Int J Mol Sci. 2017 Apr 27;18(5). pii: E920. doi: 10.3390/ijms18050920.

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

Li TM1, Liu SC2, Huang YH3, Huang CC4,5, Hsu CJ6,7, Tsai CH8,9, Wang SW10, Tang CH11,12,13.

Author information

1
School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. leedemaw@mail.cmu.edu.tw.
2
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan. sdsaw.tw@yahoo.com.tw.
3
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan. queena341@hotmail.com.
4
Division of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung 40402, Taiwan. u104054003@cmu.edu.tw.
5
Graduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan. u104054003@cmu.edu.tw.
6
School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. jeffrey5991@gmail.com.
7
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 40402, Taiwan. jeffrey5991@gmail.com.
8
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 40402, Taiwan. ritsai8615@gmail.com.
9
School of Medicine, China Medical University, Taichung 40402, Taiwan. ritsai8615@gmail.com.
10
Department of Medicine, Mackay Medical College, New Taipei City 25160, Taiwan. shihwei@mmc.edu.tw.
11
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan. chtang@mail.cmu.edu.tw.
12
School of Medicine, China Medical University, Taichung 40402, Taiwan. chtang@mail.cmu.edu.tw.
13
Department of Biotechnology, College of Health Science, Asia University, Taichung 40402, Taiwan. chtang@mail.cmu.edu.tw.

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.

KEYWORDS:

IL-18; YKL-40; angiogenesis; osteoblasts; rheumatoid arthritis

PMID:
28448439
PMCID:
PMC5454833
DOI:
10.3390/ijms18050920
[Indexed for MEDLINE]
Free PMC Article

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