Link-N: The missing link towards intervertebral disc repair is species-specific

• DOI: 10.1371/journal.pone.0187831
• Publication Date: 2017-11-08T13:33:02Z
• Authors: Frances C. Bach; Lisanne T. Laagland; Michael P. Grant; Laura B. Creemers; Keita Ito; Björn P. Meij; Fackson Mwale; Marianna A. Tryfo...
• Keywords: Intervertebral Disc

Degeneration of the intervertebral disc (IVD) is a frequent cause for back pain in humans and dogs. Link-N stabilizes proteoglycan aggregates cartilaginous tissues exerts growth factor-like effects. The human variant facilitates IVD regeneration several species vitro by inducing Smad1 signaling, but it not clear whether this specific. Dogs with disease could possibly benefit from treatment, has been tested on canine cells. If appears to be effective canines, would facilitate translation into clinic using dog as an vivo large animal model degeneration.This study's objective was determine effect short (s) chondrocyte-like cells (CLCs) compare those already studied species, i.e. bovine CLCs. Extracellular matrix (ECM) production determined measuring glycosaminoglycan (GAG) content histological evaluation. Additionally, micro-aggregates' DNA measured. Phosphorylated (p) -2 levels were ELISA.Human (s)Link-N induced GAG deposition CLCs, expected. In contrast, did affect ECM while mainly collagen type I II both negligible deposition. Surprisingly, induce Smad signaling Human only mildly increased pSmad1 Smad2 CLCs.Human exerted species-specific effects CLCs early degenerated IVDs. Both variants, however, lacked potency agent. While these studies demonstrate challenges translational models, still holds regenerative potential humans.