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Lynx Peptides

Animal & cell studies

KPV

PepT1-dependent cell uptake links KPV with NF-κB and MAP-kinase measurements. Engineered delivery adds a separate mouse-colitis research context.

Research summary

KPV stands for lysine-proline-valine, the three-residue C-terminal sequence of α-melanocyte-stimulating hormone (α-MSH). Research on this fragment should be distinguished from research on the complete hormone. PepT1 is a transporter for dipeptides and tripeptides, not a melanocortin receptor. PMID 18061177

The transport experiments ask whether KPV enters intestinal epithelial and immune cells through PepT1. NF-κB and MAP-kinase measurements then examine inflammatory signalling inside those cells. Mouse colitis experiments address a separate tissue-level question. The nanoparticle study adds a carrier and hydrogel, so it does not establish an equivalent response from free KPV. PMID 18061177 · PMID 28143741

PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation.

Gastroenterology 2008

Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D

Intestinal cells and mouse colitis models

KPV entered intestinal epithelial and immune-cell preparations through PepT1, with lower NF-κB and MAP-kinase signalling and reduced inflammatory cytokine output. In two mouse colitis models, inflammatory tissue and cytokine measures also decreased. The work connects peptide transport with intracellular signalling, while keeping cell uptake and whole-tissue responses as separate measurements.

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Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis.

Molecular therapy 2017

Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D

Cell-targeted formulation and mouse colitis model

A hyaluronic-acid-functionalised KPV nanoparticle system produced stronger intestinal inflammatory and mucosal-repair results than the comparison carrier in a mouse colitis model. Cell experiments also examined delivery to epithelial cells and macrophages. The engineered carrier and hydrogel were part of the intervention, so the result cannot be assigned to free KPV alone.

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Models studied

  • PepT1-mediated peptide transport
  • Intestinal epithelial-cell signalling
  • NF-kappaB and MAP-kinase pathways
  • Mouse colitis models

Key findings

  • Transport links with inflammatory signalling

    PepT1-dependent uptake connects KPV with inflammatory-signalling measurements in cells and mouse colitis models.

  • Why the delivery system matters

    The carrier and hydrogel form part of the KPV intervention, so its response cannot be assigned to free peptide alone.

References

  1. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation.

    Gastroenterology 2008

    Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D

    PMID 18061177

    View on PubMed

  2. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis.

    Molecular therapy 2017

    Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D

    PMID 28143741

    View on PubMed

For laboratory research use only. Content is provided for research reference and is not intended as medical or veterinary guidance.