TSG-6 Secreted by Human Umbilical cord-MSCs Attenuates Severe Burn-Induced Excessive Inflammation via Inhibiting Activations of P38 and JNK Signaling

Sci Rep. 2016 Jul 22;6:30121. doi: 10.1038/srep30121.


The hMSCs have become a promising approach for inflammation treatment in acute phase. Our previous study has demonstrated that human umbilical cord-MSCs could alleviate the inflammatory reaction of severely burned wound. In this study, we further investigated the potential role and mechanism of the MSCs on severe burn-induced excessive inflammation. Wistar rats were randomly divided into following groups: Sham, Burn, Burn+MSCs, Burn+MAPKs inhibitors, and Burn, Burn+MSCs, Burn+Vehicle, Burn+siTSG-6, Burn+rhTSG-6 in the both experiments. It was found that MSCs could only down-regulate P38 and JNK signaling, but had no effect on ERK in peritoneal macrophages of severe burn rats. Furthermore, suppression of P38 and JNK activations significantly reduced the excessive inflammation induced by severe burn. TSG-6 was secreted by MSCs using different inflammatory mediators. TSG-6 from MSCs and recombinant human (rh)TSG-6 all significantly reduced activations of P38 and JNK signaling induced by severe burn and then attenuated excessive inflammations. On the contrary, knockdown TSG-6 in the cells significantly increased phosphorylation of P38 and JNK signaling and reduced therapeutic effect of the MSCs on excessive inflammation. Taken together, this study suggested TSG-6 from MSCs attenuated severe burn-induced excessive inflammation via inhibiting activation of P38 and JNK signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Transport / drug effects
  • Burns / metabolism*
  • Cell Adhesion Molecules / metabolism*
  • Cells, Cultured
  • Humans
  • Inflammation / metabolism*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology*
  • Male
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism
  • Phosphorylation / drug effects
  • Phosphorylation / physiology
  • Protein Kinase Inhibitors / pharmacology
  • Rats
  • Rats, Wistar
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Umbilical Cord / drug effects
  • Umbilical Cord / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism*


  • Cell Adhesion Molecules
  • Protein Kinase Inhibitors
  • TNFAIP6 protein, human
  • p38 Mitogen-Activated Protein Kinases