Open AccessDown‐regulated in OA cartilage, SFMBT2 contributes to NF‐κB‐mediated ECM degradation
Author(s) -
Hussain Safdar,
Sun Mengyao,
Min Zixin,
Guo Yuanxu,
Xu Jing,
Mushtaq Nosheen,
Heng Lisong,
Huang Huang,
Zhao Yitong,
Yuan Ying,
Hussain Nazim,
Zhang Fujun,
Han Yan,
Xu Peng,
Sun Jian,
Lu Shemin
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13826
Subject(s) - anabolism , catabolism , cartilage , homeostasis , sox9 , microbiology and biotechnology , articular cartilage , nf κb , chemistry , chondrogenesis , gene , gene expression , osteoarthritis , medicine , biology , anatomy , signal transduction , pathology , biochemistry , metabolism , alternative medicine
The interplay between anabolic and catabolic factors regulates cartilage matrix homoeostasis. In OA, this balance is disrupted which results in cartilage degradation involving a plethora of inflammatory factors. Here, we identify a novel gene “Scm‐like with four MBT domains protein 2” (SFMBT2) negatively regulated in OA cartilage. Articular cartilage from human OA patients undergoing knee arthroplasty surgery exhibited significantly decreased levels of SFMBT2 compared to the normal controls. Down‐regulation of SFMBT2 by specific siRNA disturbed the metabolic homoeostasis and led to decreased expression of anabolic genes (SOX9, COL2A1) while increasing the expression of catabolic genes (MMP13 and ADAMTS4), in human chondrocytes. Finally, we revealed that SFMBT2 intervention by siRNA contributed to the catabolic phenotype of human chondrocytes mediated by NF‐kB pathway.