Wound healing with electric potential.

نویسندگان

  • Anna Huttenlocher
  • Alan Rick Horwitz
چکیده

The efficient and effective repair of damaged tissue is fundamental to human survival. Wound repair has therefore challenged generations of health care providers, and various strategies have been used to accelerate and perfect the healing process. One such strategy has involved the application of an exogenous electrical stimulus to chronic wounds with the aim of instigating electrotaxis (also called galvanotaxis). Electrotaxis — the movement of diverse cell types in response to electric gradients — has been implicated in the migration of cells to endogenous electric gradients generated in wounded tissue. Even though endogenous electric fields were first identified more than 150 years ago,1 the mechanisms that underlie electrotaxis have remained poorly understood. A recent study by Zhao et al.2 shows that common signaling pathways are able to steer cell movement in both electrical and chemical gradients. Substantial progress has been made in defining the key signaling components that mediate chemotaxis, the directed migration of cells in gradients of a chemoattractant. A series of studies by investigators using both the slime mold Dictyostelium discoideum and leukocytes have shown that the sensing of chemical gradients involves the asymmetric recruitment of signaling and cytoskeletal components that mediate cell polarization and directed movement.3,4 A critical event in gradient sensing during chemotaxis is the recruitment of phosphatidylinositol 3,4,5-triphosphate (PIP3) to the part of the cell that faces the gradient of chemoattractant. The pathway that is mediated by phosphatidylinositol 3-kinase (PI3K) has been implicated in the polarization and chemotaxis of diverse cell types exposed to chemical gradients (Fig. 1). A key role of PIP3 signaling is also supported by the importance of the tumorsuppressor phosphatase and tensin homologue (PTEN) during chemotaxis. PTEN is a lipid phosphatase that negatively regulates the generation of PIP3; it is recruited to the trailing portion of D. discoideum during chemotaxis and serves to enhance the concentration of PIP3 at the front. Abrogation of PTEN in slime mold cells reduces the efficiency of chemotaxis, again supporting a critical role of the asymmetric regulation of phosphoinositide signaling during chemotaxis. The work of Zhao et al. suggests that the tension between PTEN and PI3K is also relevant to electrotaxis in wound healing. The researchers tested the effect of removing phosphoinositidesignaling components on both directional sensing and migration of keratinocytes. They used gradients of electric potential of the same magnitude as those observed in endogenous settings

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عنوان ژورنال:
  • The New England journal of medicine

دوره 356 3  شماره 

صفحات  -

تاریخ انتشار 2007