Maggot excretions/secretions induces human microvascular endothelial cell migration through AKT1.
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.
Wang
Shou-yu
SY
Department of Orthopaedics, The First Affiliated Hospital of Dalian Medical University, 222 Zhong Shan Road, 116011, Dalian, Liaoning, People's Republic of China.
Wang
Kai
K
Xin
Yi
Y
Lv
De-cheng
DC
D000818:Animals; D002465:Cell Movement; D002470:Cell Survival; D042783:Endothelial Cells / Q000166:cytology* / Q000201:enzymology*; D004789:Enzyme Activation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D007313:Insecta / Q000254:growth & development*; D007814:Larva / Q000378:metabolism; D055806:Microvessels / Q000166:cytology*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D014945:Wound Healing
D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases