HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

Flightless I is a catabolic factor of chondrocytes that promotes hypertrophy and cartilage degeneration in osteoarthritis

Files in This Item:

The file(s) associated with this item can be obtained from the following URL:

Title: Flightless I is a catabolic factor of chondrocytes that promotes hypertrophy and cartilage degeneration in osteoarthritis
Authors: Ebata, Taku Browse this author
Terkawi, Mohamad Alaa Browse this author
Hamasaki, Masanari Browse this author
Matsumae, Gen Browse this author
Onodera, Tomohiro Browse this author →KAKEN DB
Aly, Mahmoud Khamis Browse this author
Yokota, Shunichi Browse this author
Alhasan, Hend Browse this author
Shimizu, Tomohiro Browse this author
Takahashi, Daisuke Browse this author
Homan, Kentaro Browse this author
Kadoya, Ken Browse this author
Iwasaki, Norimasa Browse this author →KAKEN DB
Issue Date: 25-Jun-2021
Publisher: Cell Press
Journal Title: iScience
Volume: 24
Issue: 6
Start Page: 102643
Publisher DOI: 10.1016/j.isci.2021.102643
Abstract: Synovial macrophages that are activated by cartilage fragments initiate synovitis, a condition that promotes hypertrophic changes in chondrocytes leading to cartilage degeneration in OA. In this study, we analyzed the molecular response of chondrocytes under condition of this type of stimulation to identify a molecular therapeutic target. Stimulated macrophages promoted hypertrophic changes in chondrocytes resulting in production of matrix-degrading enzymes of cartilage. Among the top-upregulated genes, FliI was found to be released from activated chondrocytes and exerted autocrine/paracrine effects on chondrocytes leading to an increase in expression of catabolic and hypertrophic factors. Silencing FliI in stimulated cells significantly reduced expression of catabolic and hypertrophic factors in cocultured chondrocytes. Our further results demonstrated that the FliI-TLR4-ERK1/2 axis is involved in the hypertrophic signaling of chondrocytes and catabolism of cartilage. Our findings provide a new insight into the pathogenesis of OA and identify a potentially new molecular target for diagnostics and therapeutics.
Type: article
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 - Hokkaido University