Related Experiment Video

Updated: Jan 13, 2026

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
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Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients

Published on: October 16, 2016

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PLSCR1 Regulates the Physiology of Fibroblast-Like Synoviocytes via Modulating the STAT1 Signaling Pathway

Tianhua Chen1, Jiaojiao Wang2

  • 1Department of Pain Management, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan, China.

Immunity, Inflammation and Disease
|October 28, 2025
PubMed
Abstract

Insights

Phospholipid scramblase 1 (PLSCR1) is elevated in rheumatoid arthritis (RA) patients. It drives inflammation and joint damage by affecting fibroblast-like synoviocyte (FLS) proliferation and apoptosis via the STAT1 pathway, suggesting PLSCR1 as a therapeutic target.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) involves chronic synovial inflammation and joint destruction.
  • Understanding RA pathogenesis is key to developing new therapies.
  • Phospholipid scramblase 1 (PLSCR1) is linked to autoimmune diseases, but its role in RA is unknown.

Purpose of the Study:

  • To investigate the role and mechanism of PLSCR1 in rheumatoid arthritis.
  • To determine if PLSCR1 is a potential therapeutic target for RA.

Main Methods:

  • Quantified PLSCR1 serum expression in RA patients versus healthy controls using RT-qPCR.
  • Assessed PLSCR1 function in human fibroblast-like synoviocytes (HFLSs) via siRNA knockdown.
  • Measured HFLS proliferation, apoptosis, and cytokine release (TNF-α, IL-1β, IL-6); explored PLSCR1-STAT1 interaction.

Main Results:

  • PLSCR1 serum levels were significantly higher in RA patients.
  • PLSCR1 knockdown in HFLSs reduced proliferation, increased apoptosis, and lowered inflammatory cytokine levels.
  • PLSCR1 knockdown also decreased STAT1 expression; STAT1 activation reversed these effects.

Conclusions:

  • PLSCR1 is upregulated in RA and influences FLS proliferation, apoptosis, and inflammation through the STAT1 pathway.
  • PLSCR1 represents a potential molecular target for rheumatoid arthritis treatment.
Keywords:
PLSCR1STAT1fibroblast‐like synoviocytesrheumatoid arthritis

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