Related Experiment Video

Updated: Aug 17, 2026

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
09:31

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

Published on: October 16, 2016

Human synovial fibroblast plasminogen activator. Modulation of enzyme activity by antiinflammatory steroids

J H Hamilton, A Bootes, P E Phillips

    Arthritis and Rheumatism
    |October 1, 1981
    PubMed

    Insights

    Anti-inflammatory steroids, like dexamethasone, can inhibit plasminogen activator (PA) activity in human synovial fibroblasts. This suggests a potential mechanism for controlling inflammation and tissue remodeling in vivo.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Immunology

    Background:

    • Human synovial fibroblasts exhibit low basal plasminogen activator (PA) activity.
    • Concanavalin A-stimulated peripheral blood mononuclear cell conditioned medium (c-MCCM) enhances PA levels in these cells.

    Purpose of the Study:

    • To investigate the effect of anti-inflammatory steroids on PA activity in human synovial fibroblasts.
    • To determine if dexamethasone influences extracellular and cell-associated PA activities.

    Main Methods:

    • Fibroblast cultures were treated with varying concentrations of anti-inflammatory steroids.
    • PA activity was measured in both unstimulated and c-MCCM-stimulated fibroblasts.
    • Effects on cellular RNA, protein, and DNA synthesis were assessed.

    Main Results:

    • Low concentrations of anti-inflammatory steroids, including dexamethasone, inhibited PA activity in both unstimulated and stimulated fibroblasts.
    • Dexamethasone rapidly and reversibly suppressed both extracellular and cell-associated PA activities.
    • This inhibition was independent of effects on cellular nucleic acid or protein synthesis.

    Conclusions:

    • Glucocorticoids, such as dexamethasone, can effectively modulate plasminogen activator levels in synovial fibroblasts.
    • These findings suggest a potential in vivo mechanism involving the interplay between mononuclear cell products and glucocorticoids for controlling synovial fibroblast PA activity.
    • This modulation may have implications for managing inflammatory and tissue remodeling processes.

    More Related Videos

    Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue09:18

    Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue

    Published on: February 24, 2023

    A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture08:32

    A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture

    Published on: March 20, 2026

    Related Concept Videos

    The JAK-STAT Signaling Pathway01:20

    The JAK-STAT Signaling Pathway

    Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
    Inflammatory Response01:28

    Inflammatory Response

    An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
    Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
    Acute Inflammation III: Local and Systemic Effects01:25

    Acute Inflammation III: Local and Systemic Effects

    Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
    Chronic Inflammation: Introduction01:12

    Chronic Inflammation: Introduction

    Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...