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.
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
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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