Maggot excretions/secretions induces human microvascular endothelial cell migration through AKT1

Mol Biol Rep. 2010 Jul;37(6):2719-25. doi: 10.1007/s11033-009-9806-x. Epub 2009 Sep 16.


Maggot therapy is a simple and highly successful method for healing of infected and necrotic wounds. The increasing evidences indicate that Maggot excretions/secretions (ES) plays important roles in the wounds healing process. But the precise molecular mechanisms remain undefined. Herein, we investigated if ES induced cell migration during wound healing process using microvascular endothelial cells (HMEC-1) as model, and this effect was associated with the activation of AKT1 and ERK1/2. Wound healing and transwell migration assays were performed to study the effects of ES on HMEC-1 cell migration. Our data showed that ES significantly induced HMEC-1 cell migration in both wound healing and transwell assays, and time-dependently (P < 0.05) activated AKT1, but not ERK1/2. Moreover LY294002 (a PI3K inhibitor) partially attenuated (P < 0.05) ES-induced cell migration in wound healing assay while completely inhibited (P < 0.05) ES-induced AKT1 activation. These findings demonstrate that ES directly induces HMEC-1 cell migration and this event is partially mediated by the activation of AKT1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Movement*
  • Cell Survival
  • Endothelial Cells / cytology*
  • Endothelial Cells / enzymology*
  • Enzyme Activation
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Insecta / growth & development*
  • Larva / metabolism
  • Microvessels / cytology*
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Wound Healing


  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases