Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

A Metalloproteinase Induces an Inflammatory Response in Preadipocytes with the Activation of COX Signalling Pathways and Participation of Endogenous Phospholipases A 2

Janovits PM., Leiguez E., Portas V., Teixeira C.

Animal Study on Chronic Inflammation, published in Biomolecules (2021) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Biomolecules (2021)
Reported sample size
—
Source database
Europe PMC
PMID
34206390
PMCID
PMC8301905
DOI
10.3390/biom11070921
Citations
5

Abstract (original English)

Matrix metalloproteinases (MMPs) are proteolytic enzymes that have been associated with the pathogenesis of inflammatory diseases and obesity. Adipose tissue in turn is an active endocrine organ capable of secreting a range of proinflammatory mediators with autocrine and paracrine properties, which contribute to the inflammation of adipose tissue and adjacent tissues. However, the potential inflammatory effects of MMPs in adipose tissue cells are still unknown. This study investigates the effects of BmooMPα-I, a single-domain snake venom metalloproteinase (SVMP), in activating an inflammatory response by 3T3-L1 preadipocytes in culture, focusing on prostaglandins (PGs), cytokines, and adipocytokines biosynthesis and mechanisms involved in prostaglandin E 2 (PGE 2 ) release. The results show that BmooMPα-I induced the release of PGE 2 , prostaglandin I 2 (PGI 2 ), monocyte chemoattractant protein-1 (MCP-1), and adiponectin by preadipocytes. BmooMPα-I-induced PGE 2 biosynthesis was dependent on group-IIA-secreted phospholipase A 2 (sPLA 2 -IIA), cytosolic phospholipase A 2 -α (cPLA 2 -α), and cyclooxygenase (COX)-1 and -2 pathways. Moreover, BmooMPα-I upregulated COX-2 protein expression but not microsomal prostaglandin E synthase-1 (mPGES-1) expression. In addition, we demonstrate that the enzymatic activity of BmooMPα-I is essential for the activation of prostanoid synthesis pa

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
3T3-L1 CellsAdipocytesAnimalsMiceInflammationMetalloendopeptidasesDinoprostoneCrotalid VenomsSignal TransductionProstaglandin-Endoperoxide Synthases

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