Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMedOpen access

Proteomic profiling of adipose-derived mesenchymal stromal cell response to novel compounds targeting the Laminin Receptor - PEDF interaction.

Figueiredo ML., Figueiredo Neto M., Umbaugh CS., Sobreira TJP., Elsbury CE., Mulia GE.

Laboratory Study on Cartilage Damage, Chronic Inflammation, published in Biochem Biophys Rep (2025) — 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
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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
Laboratory Study
Journal
Biochem Biophys Rep (2025)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
41378102
PMCID
PMC12686635
DOI
10.1016/j.bbrep.2025.102377

Abstract (original English)

This study characterizes the proteomic responses of adipose-derived mesenchymal stromal cells (ASC) to novel compounds that target the interaction between pigment epithelium-derived factor (PEDF) and the 37 KDa Laminin Receptor (LR). Building on previous research, we introduced the second-generation analog, 02-09, for comparative analysis with C3, the original compound. C3 was identified through in silico screening and experimental validation, showing anti-inflammatory activity. Analog 02-09 was synthesized by modifying C3's aromatic ring, resulting in similar binding affinities to LR. The distinct molecular effects of C3 and 02-09, along with their potential as anti-inflammatory therapies from prior work, suggested their multi-functional utility. Proteomic profiling of ASC, under both undifferentiated and chondrogenic differentiation conditions, was performed using LC-MS/MS, with controls including the PEDF-derived peptide p18 and the cartilage-regenerative compound Kartogenin (Krt). Both C3 and 02-09 induced significant proteomic modulation compared to controls, with enrichment in pathways related to integrin β1 signaling, extracellular matrix (ECM) organization , and TGF-β signaling . C3 uniquely activated the nuclear receptors meta-pathway, whereas 02-09 was associated with laminin interactions . Protein-protein interaction and transcription factor enrichment analyses revea

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.

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