title: Protein kinase B/AKT isoform 2 drives migration of human mesenchymal             stem cells.
abstract: This study was designed to investigate the migratory behavior of adult human             mesenchymal stem cells (MSC) and the underlying mechanism. Cell migration was             assessed by transwell, wound healing and time-lapse in vivo motility assays. Pharmacological             inhibitors were used to determine the potential mechanism responsible for cell             migration and invasion. The tests that were implemented revealed that MSC were             fairly migratory. Protein kinase B (AKT) was strongly activated at the basal level.             Through our analyses we demonstrated that pharmacological inactivation of AKT2             but not AKT1 significantly decreased cell migration and invasion. Although preliminary,             collectively our results indicate that AKT2 activation plays a critical role in             enabling MSC migration.
authors.affiliation: Department of Biomedical Sciences, Cellular Signalling Laboratory, Bologna, Italy.
authors.forename: Zrinka
authors.initials: Z
authors.lastname: Bulj
authors.forename: Serena
authors.initials: S
authors.lastname: Duchi
authors.forename: Alessandro
authors.initials: A
authors.lastname: Bevilacqua
authors.forename: Alessandro
authors.initials: A
authors.lastname: Gherardi
authors.forename: Barbara
authors.initials: B
authors.lastname: Dozza
authors.forename: Filippo
authors.initials: F
authors.lastname: Piccinini
authors.forename: Giulia
authors.initials: G
authors.lastname: Adalgisa Mariani
authors.forename: Enrico
authors.initials: E
authors.lastname: Lucarelli
authors.forename: Sandro
authors.initials: S
authors.lastname: Giannini
authors.forename: Davide
authors.initials: D
authors.lastname: Donati
authors.forename: Sandra
authors.initials: S
authors.lastname: Marmiroli
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002448:Cell Adhesion / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002867:Chromones / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005434:Flow Cytometry; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D009025:Morpholines / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014945:Wound Healing / Q000187:drug effects
chemical_list: D002867:Chromones; D004791:Enzyme Inhibitors; D009025:Morpholines; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; C494918:AKT1 protein, human; C494921:AKT2 protein, human