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 investi...

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Published inMolecular biology reports Vol. 37; no. 6; pp. 2719 - 2725
Main Authors Wang, Shou-yu, Wang, Kai, Xin, Yi, Lv, De-cheng
Format Journal Article
LanguageEnglish
Published Dordrecht Dordrecht : Springer Netherlands 01.07.2010
Springer Netherlands
Springer Nature B.V
Subjects
AKT1
Animal Anatomy
Animal Biochemistry
Animals
Biomedical and Life Sciences
Cell adhesion & migration
Cell Movement
Cell Survival
Endothelial Cells - cytology
Endothelial Cells - enzymology
Enzyme Activation
Extracellular Signal-Regulated MAP Kinases - metabolism
Histology
HMEC-1
Humans
Inhibitor drugs
Insecta - growth & development
Insects
Larva - metabolism
Life Sciences
Microvessels - cytology
Migration
Molecular biology
Morphology
Phosphorylation
Proto-Oncogene Proteins c-akt - metabolism
tissue repair
Wound Healing
AKT1
Wound healing
HMEC-1
Migration
ES
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Summary: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.
Bibliography:http://dx.doi.org/10.1007/s11033-009-9806-x
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ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-009-9806-x