NFIC attenuates rheumatoid arthritis-induced inflammatory response in mice by regulating PTEN/SENP8 transcription

  • Tissue Cell. 2023 Apr:81:102013. doi: 10.1016/j.tice.2023.102013.
Pengfei Jia  1 ,  Wen Zhang  1 ,  Yongyan Shi  2
Affiliations
  • 1. Department of Spinal Surgery, Suizhou Central Hospital, Hubei University of Medicine, Suizhou, Hubei 441300, PR China.
  • 2. Department of Spinal Surgery, Suizhou Central Hospital, Hubei University of Medicine, Suizhou, Hubei 441300, PR China. Electronic address: [email protected].
PMID: 36669387 DOI: 10.1016/j.tice.2023.102013
Abstract

Objective: To explore whether nuclear factor I C (NFIC) alleviated inflammatory response of synovial fibroblasts (SFs) caused by Rheumatoid Arthritis (RA) by regulating transcription levels of Phosphatase and tension homolog deleted on chromosome 10 (PTEN) and sentrin-specific Protease 8 (SENP8).

Methods: NFIC, PTEN, and SENP8 levels in RASFs and normal SFs (NSFs) were measured by qRT-PCR and western blotting. The levels of Bax, Bcl-2, MMP-3, and MMP-13, as well as the content of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined in RASFs and NSFs using western blotting and ELISA. The binding of NFIC to promoter sequences of PTEN and SENP8 was predicted and verified. A mouse model of collagen-induced Arthritis (CIA) was established and evaluated according to the degree of joint swelling and Arthritis index.

Results: NFIC, PTEN, and SENP8 were downregulated in RASFs. RASFs had increased viability and MDA levels as well as decreased cell Apoptosis and SOD content. NFIC was demonstrated to modulate the transcription of PTEN and SENP8 as their transcription factor. NFIC ameliorated the inflammatory response induced by RA in vivo by promoting the transcription of PTEN and SENP8.

Conclusion: NFIC acted as a transcription factor to facilitate the transcription of PTEN and SENP8, thereby inducing Apoptosis of RASFs and effectively attenuating inflammatory response in CIA mice.

Keywords
Mouse model of collagen-induced arthritis; Nuclear Factor I C; Phosphatase and tension homolog deleted on chromosome 10; Rheumatoid arthritis; Sentrin-specific protease 8; Transcription factor.
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