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

Ebata, Taku; Terkawi, Mohamad Alaa; Hamasaki, Masanari et al.

iScience, 2021, 24(6), 102643

Permalink : https://hdl.handle.net/2115/82552

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https://doi.org/10.1016/j.isci.2021.102643     13

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アクセス権
open access
URI
https://hdl.handle.net/2115/82552
タイトル
Flightless I is a catabolic factor of chondrocytes that promotes hypertrophy and cartilage degeneration in osteoarthritis
著者
Ebata, Taku ; Terkawi, Mohamad Alaa ; Hamasaki, Masanari ; Matsumae, Gen ; Onodera, Tomohiro ; Aly, Mahmoud Khamis ; Yokota, Shunichi ; Alhasan, Hend ; Shimizu, Tomohiro ; Takahashi, Daisuke ; Homan, Kentaro ; Kadoya, Ken ; Iwasaki, Norimasa
著者名
Ebata, Taku
著者名
Terkawi, Mohamad Alaa
著者名
Hamasaki, Masanari
著者名
Matsumae, Gen
e-Rad_Researcher
70547174
著者名
Onodera, Tomohiro
著者名
Aly, Mahmoud Khamis
著者名
Yokota, Shunichi
著者名
Alhasan, Hend
著者名
Shimizu, Tomohiro
著者名
Takahashi, Daisuke
著者名
Homan, Kentaro
著者名
Kadoya, Ken
e-Rad_Researcher
30322803
著者名
Iwasaki, Norimasa
言語
英語
発行日
2021-06-25
出版者
Cell Press
収録物名
iScience
巻(号)
24(6)
ページ
102643
抄録
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.
資源タイプ
学術雑誌論文
出版タイプ
Version of Record
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出版社版DOI
https://doi.org/10.1016/j.isci.2021.102643