Electrical Signals Control Wound Healing Through Phosphatidylinositol-3-oh Kinase-gamma and Pten.
From: School of Medical Sciences and Department of Ophthalmology, University of Aberdeen, Aberdeen AB25 2ZD, UK. m.zhao@abdn.ac.uk
Nature
- Publish Date: Jul 2006
- ISSN: 1476-4687
- Volume: 442
- Issue: 7101
- Pages: 457-60
- Medium: Internet
- Language: English
- Citation (JAMA): Zhao Min, Song Bing, Pu Jin, et al. Electrical Signals Control Wound Healing Through Phosphatidylinositol-3-oh Kinase-gamma and Pten.. Nature Jul 2006;442:457-60
Abstract
Wound healing is essential for maintaining the integrity of multicellular organisms. In every species studied, disruption of an epithelial layer instantaneously generates endogenous electric fields, which have been proposed to be important in wound healing. The identity of signalling pathways that guide both cell migration to electric cues and electric-field-induced wound healing have not been elucidated at a genetic level. Here we show that electric fields, of a strength equal to those detected endogenously, direct cell migration during wound healing as a prime directional cue. Manipulation of endogenous wound electric fields affects wound healing in vivo. Electric stimulation triggers activation of Src and inositol-phospholipid signalling, which polarizes in the direction of cell migration. Notably, genetic disruption of phosphatidylinositol-3-OH kinase-gamma (PI(3)Kgamma) decreases electric-field-induced signalling and abolishes directed movements of healing epithelium in response to electric signals. Deletion of the tumour suppressor phosphatase and tensin homolog (PTEN) enhances signalling and electrotactic responses. These data identify genes essential for electrical-signal-induced wound healing and show that PI(3)Kgamma and PTEN control electrotaxis.
Mesh Headings (Keywords): 1-Phosphatidylinositol 3-Kinase, Animals, Cell Movement, Dictyostelium, Electric Stimulation, Isoenzymes, Mice, PTEN Phosphohydrolase, Signal Transduction, Wound Healing
Check for Full Text / PubMed Unique Identifier (PMID): 16871217
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