[Stromelysin-1 in inflammatory disease: significance, specificity, and regulation elements]

C Ribbens1, M Malaise

  • 1Université de Liège, Centre hospitalier universitaire du Sart-Tilman, Service de Rhumatologie, Centre d'Etude des Maladies inflammatoires chroniques.

Bulletin Et Memoires De L'Academie Royale De Medecine De Belgique
|April 4, 2002
PubMed

Insights

Matrix metalloproteinase-3 (MMP-3) is a key enzyme in rheumatoid arthritis joint degradation. Serum MMP-3 may serve as a valuable marker for predicting disease activity and treatment response.

Area of Science:

  • Biochemistry
  • Immunology
  • Rheumatology

Context:

  • Rheumatoid arthritis (RA) involves extracellular matrix degradation.
  • Pro-inflammatory cytokines induce matrix metalloproteinase-3 (MMP-3).
  • MMP-3 activates other metalloproteinases and reflects local inflammation.

Purpose:

  • To evaluate the role of MMP-3 as a marker in rheumatoid arthritis.
  • To assess MMP-3's potential in predicting disease activity and therapeutic response.

Summary:

  • Stromelysin-1 (MMP-3) is crucial in RA extracellular matrix breakdown.
  • Serum MMP-3 levels increase with synovitis and steroid therapy.
  • While not specific to RA, MMP-3 is a useful synovial marker for local inflammation.

Impact:

  • Serum MMP-3 can be a valuable tool for monitoring RA.
  • Early MMP-3 determination may predict disease activity and treatment outcomes.
  • MMP-3 offers a parallel marker to CRP for assessing inflammation in RA.

Related Concept Videos

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,...
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...
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...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...