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.
Bulj Z, Duchi S, Bevilacqua A, Gherardi A, Dozza B, Piccinini F, et al. (2013). Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells. INTERNATIONAL JOURNAL OF ONCOLOGY, 42(1), 118-126 [10.3892/ijo.2012.1700].
Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells.
BULJ, ZRINKA;DUCHI, SERENA;BEVILACQUA, ALESSANDRO;GHERARDI, ALESSANDRO;DOZZA, BARBARA;PICCININI, FILIPPO;MARIANI, GIULIA ADALGISA;GIANNINI, SANDRO;DONATI, DAVIDE MARIA;
2013
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
