KPV

Zhao Y, Huang L, Lin G, Tong M, Xie Y, Pan H, et al.

International journal of biological macromolecules

In a diabetic mouse full-thickness skin wound model, researchers incorporated the tripeptide KPV together with epidermal growth factor into a layered adhesive film dressing and studied its effects on wound repair. Improved repair rates were associated with reduced inflammatory signaling, increased angiogenesis, and increased collagen deposition at the wound site.

Shao W, Chen R, Lin G, Ran K, Zhang Y, Yang J, et al.

Biomaterials science

Using a rat model of chemotherapy-induced oral mucosal injury, researchers formulated tripeptide KPV in a mucoadhesive, temperature-responsive hydrogel and observed reduced pro-inflammatory cytokines (IL-1β, TNF-α) with increased IL-10, together with antibacterial activity against Staphylococcus aureus and improved epithelial tissue morphology at the ulcerated site.

Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, et al.

Molecular therapy : the journal of the American Society of Gene Therapy

In a mouse model of ulcerative colitis, hyaluronic-acid-functionalized nanoparticles were engineered to deliver KPV to colonic epithelial cells and macrophages. KPV delivery was associated with reduced TNF-α expression and accelerated mucosal repair relative to untreated colitis controls, with nanoparticles shown to be non-toxic to intestinal cells in vitro.

Land SC

International journal of physiology, pathophysiology and pharmacology

In cultured human bronchial epithelial cells (16HBE14o-), KPV inhibited TNFα- and respiratory-syncytial-virus-evoked NF-κB signaling. This effect was linked to blockade of nuclear import of the p65RelA subunit via an interaction with the importin-α3 binding site, alongside reduced secretion of the chemokines IL-8 and eotaxin, outlining a mechanism distinct from the MC3R-mediated pathway used by gamma-MSH in the same model.

Elliott RJ, Szabo M, Wagner MJ, Kemp EH, MacNeil S, Haycock JW

The Journal of investigative dermatology

In human keratinocyte cell lines (HaCaT and primary keratinocytes) and melanocortin-1-receptor-transfected CHO cells, alpha-MSH, the tripeptide KPV, and related peptides (KP-D-V, ACTH fragments) did not elevate cyclic AMP, but produced rapid, transient intracellular calcium signaling when co-treated with an adenosine-receptor agonist (PIA) that blocks the cyclic AMP pathway. The findings characterized a calcium-linked, cyclic-AMP-independent signaling route at the melanocortin-1 receptor for this C-terminal alpha-MSH fragment.