USF1 promotes the development of knee osteoarthritis by activating the NF‑κB signaling pathway

Abstract

The current study mainly aims to evaluate the expression pattern and underlying mechanism of upstream stimulating factor 1 (USF1) in the muscle tissues of knee osteoarthritis (KOA) patients. In accordance with previous findings, our data showed that muscle strength was significantly decreased in KOA patients compared with controls. Furthermore, several inflammatory factors, including tumor necrosis factor α (TNFα), IL-8, IL-6 and MCP-1, were associated with reduced muscle strength in KOA patients. Not surprisingly, NF-κB signaling was significantly activated in the muscle tissues of KOA patients compared with control individuals. Furthermore, we showed that USF1 was increased in the muscles of KOA patients compared with controls. More importantly, overexpression of USF1 in primary human skeletal muscle cells significantly increased the activation of NF-κB signaling as well as the levels of pro-inflammatory factors. In summary, we showed novel data that the upregulation of USF1 promoted NF-κB activation-induced inflammatory responses in muscle tissues of KOA patients.

Association of the Expression Levels of Long-Chain Noncoding RNA TUG1 and Its Gene Polymorphisms with Knee Osteoarthritis

“…It is acknowledged that synovitis is common in early KOA and is associated with knee pain and cartilage degeneration and defects. Some inflammatory cytokines, such as IL-6, IL-8, nuclear factor kB (NF-kB), and adipokines can be detected in early KOA, indicating that these factors may correlate with the occurrence and development of KOA (Song et al, 2018;Sun et al, 2019). The lncRNA/microRNA/mRNA regulatory axis plays a vital role in the occurrence and development of diseases, but whether lncRNA TUG1 participates in the occurrence and development of KOA through microRNA regulating IL-6, IL-8, NF-kB, and adipokines require further research.…”

Up‐regulation of ZFAS1 indicates dismal prognosis for cholangiocarcinoma and promotes proliferation and metastasis by modulating USF1 via miR‐296‐5p

“…USF1 has been evaluated as transcription factor that could bind gene-specific binding motif in the previous research and activated gene expression. 34 Consequentially, we attempted with the help of JASPAR and discovered that USF1 might be an important transcription factor for ZFAS1. In addition to that results, the associative property of USF1 on the motifs of CCA-related lncRNAs was also evaluated.…”

A natural variation-based screen in mouse cells reveals USF2 as a regulator of the DNA damage response and cellular senescence

“…It is tempting to speculate that USF2 ultimately works in these processes in concert with its better-studied family member, USF1. Indeed, USF1 has been implicated in DNA repair ( Baron et al 2012 ), inflammation ( Ruuth et al 2018 ; Song et al 2018 ), immune responses ( Corre and Galibert 2005 ), and p53-mediated cell cycle arrest ( Bouafia et al 2014 ) in contexts other than senescence. In addition, given that USF2 has been implicated in the TGFβ-p53 axis in apoptosis ( Sato et al 2011 ) and fibrosis ( Samarakoon et al 2012 ), the latter pathway could mediate some part of the USF2 effects we have seen.…”