%0 Journal Article %1 meng2011mediated %A Meng, Xiaoting %A Arocena, Miguel %A Penninger, Josef %A Gage, Fred H. %A Zhao, Min %A Song, Bing %D 2011 %J Experimental Neurology %K efield migration npc phd stemcell %N 1 %P 210--217 %R 10.1016/j.expneurol.2010.11.002 %T \PI3K\ mediated electrotaxis of embryonic and adult neural progenitor cells in the presence of growth factors %U http://www.sciencedirect.com/science/article/pii/S0014488610004036 %V 227 %X Correct guidance of the migration of neural progenitor cells (NPCs) is essential for the development and repair of the central nervous system (CNS). Electric field (EF)-guided migration, electrotaxis, has been observed in many cell types. We report here that, in applied \EFs\ of physiological magnitude, embryonic and adult \NPCs\ show marked electrotaxis, which is dependent on the PI3K/Akt pathway. The electrotaxis was also evidenced by ex vivo investigation that transplanted \NPCs\ migrated directionally towards cathode in organotypic spinal cord slice model when treated with EFs. Genetic disruption or pharmacological inhibition of phosphoinositide 3-kinase (PI3K) impaired electrotaxis, whereas \EF\ exposure increased Akt phosphorylation in a growth factor-dependent manner and increased phosphatidylinositol-3,4,5-trisphosphate (PIP3) levels. \EF\ treatments also induced asymmetric redistribution of PIP3, growth factor receptors, and actin cytoskeleton. Electrotaxis in both embryonic and adult \NPCs\ requires epidermal growth factor (EGF) and fibroblast growth factor (FGF). Our results demonstrate the importance of the PI3K/Akt pathway in directed migration of \NPCs\ driven by \EFs\ and growth factors and highlight the potential of \EFs\ to enhance the guidance of various \NPC\ populations in \CNS\ repair therapies.

@article{meng2011mediated, abstract = {Correct guidance of the migration of neural progenitor cells (NPCs) is essential for the development and repair of the central nervous system (CNS). Electric field (EF)-guided migration, electrotaxis, has been observed in many cell types. We report here that, in applied \{EFs\} of physiological magnitude, embryonic and adult \{NPCs\} show marked electrotaxis, which is dependent on the PI3K/Akt pathway. The electrotaxis was also evidenced by ex vivo investigation that transplanted \{NPCs\} migrated directionally towards cathode in organotypic spinal cord slice model when treated with EFs. Genetic disruption or pharmacological inhibition of phosphoinositide 3-kinase (PI3K) impaired electrotaxis, whereas \{EF\} exposure increased Akt phosphorylation in a growth factor-dependent manner and increased phosphatidylinositol-3,4,5-trisphosphate (PIP3) levels. \{EF\} treatments also induced asymmetric redistribution of PIP3, growth factor receptors, and actin cytoskeleton. Electrotaxis in both embryonic and adult \{NPCs\} requires epidermal growth factor (EGF) and fibroblast growth factor (FGF). Our results demonstrate the importance of the PI3K/Akt pathway in directed migration of \{NPCs\} driven by \{EFs\} and growth factors and highlight the potential of \{EFs\} to enhance the guidance of various \{NPC\} populations in \{CNS\} repair therapies. }, added-at = {2013-08-29T13:36:14.000+0200}, author = {Meng, Xiaoting and Arocena, Miguel and Penninger, Josef and Gage, Fred H. and Zhao, Min and Song, Bing}, biburl = {https://www.bibsonomy.org/bibtex/225267f489ecd9b3d1df1e89c9ee78c1a/bkoch}, description = {PI3K mediated electrotaxis of embryonic and adult neural progenitor cells in the presence of growth factors}, doi = {10.1016/j.expneurol.2010.11.002}, interhash = {154423cdf51dbd2faccbe6049ee69f33}, intrahash = {25267f489ecd9b3d1df1e89c9ee78c1a}, issn = {0014-4886}, journal = {Experimental Neurology }, keywords = {efield migration npc phd stemcell}, number = 1, pages = {210--217}, timestamp = {2013-08-29T13:36:14.000+0200}, title = {\{PI3K\} mediated electrotaxis of embryonic and adult neural progenitor cells in the presence of growth factors }, url = {http://www.sciencedirect.com/science/article/pii/S0014488610004036}, volume = 227, year = 2011 }