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Intervening upregulated SLC7A5 could mitigate inflammatory mediator by mTOR-P70S6K signal in rheumatoid arthritis

Jing Xu1,2, Congshan Jiang1,2, Yongsong Cai3

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, People's Republic of China.

Arthritis Research & Therapy
|September 2, 2020
PubMed
Abstract

Insights

The study reveals that the NF-κB pathway activates SLC7A5 in rheumatoid arthritis (RA) fibroblast-like synoviocytes. This increases mTOR activity and matrix metalloproteinase (MMP) expression, contributing to RA pathogenesis.

Area of Science:

  • Rheumatology
  • Molecular Biology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) involves sustained inflammation, altering cellular metabolism and nutrient availability.
  • This metabolic disruption increases demands on bioenergetic and biosynthetic processes in affected tissues.
  • Understanding molecular mechanisms in RA synoviocytes is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the molecular mechanisms of the solute carrier family 7 member 5 (SLC7A5) amino acid transporter in rheumatoid arthritis (RA) patients.
  • To elucidate the role of SLC7A5 in regulating cellular processes within synoviocytes.

Main Methods:

  • Synovial tissues from osteoarthritis (OA) and RA patients were analyzed.
  • Fibroblast-like synoviocytes (FLS) were isolated and SLC7A5 expression was quantified using RT-qPCR, immunofluorescence, and Western blotting.
  • RNA interference (RNAi), antibody blocking, mTOR activity assays, and matrix metalloproteinase (MMP) expression monitoring were employed.

Main Results:

  • SLC7A5 expression was significantly upregulated in RA FLS compared to OA FLS.
  • The cytokine IL-1β, via the NF-κB pathway, was identified as a key regulator of SLC7A5 expression.
  • Intervention targeting SLC7A5 ameliorated MMP3 and MMP13 expression, while its upregulation enhanced mTOR signaling and MMP production.

Conclusions:

  • The activated NF-κB pathway upregulates SLC7A5 in RA FLS.
  • SLC7A5 enhances mTOR-P70S6K activity, promoting MMP3 and MMP13 expression.
  • Targeting SLC7A5 presents a potential therapeutic strategy for RA.
Keywords:
Fibroblast-like synoviocytesMMPsRheumatoid arthritisSLC7A5mTOR-P70S6K

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