Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells

Zrinka Bulj; Serena Duchi; Alessandro Bevilacqua; Alessandro Gherardi; Barbara Dozza; Filippo Piccinini; Giulia Adalgisa Mariani; Enrico Lucarelli; Sandro Giannini; Davide Donati; Sandra Marmiroli

doi:10.3892/ijo.2012.1700

Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells

Zrinka Bulj, Serena Duchi, Alessandro Bevilacqua, Alessandro Gherardi, Barbara Dozza, Filippo Piccinini, Giulia Adalgisa Mariani, Enrico Lucarelli, Sandro Giannini, Davide Donati, Sandra Marmiroli

Research output: Contribution to journal › Article › peer-review

22 Scopus citations

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.

Original language	English (US)
Pages (from-to)	118-126
Number of pages	9
Journal	International Journal of Oncology
Volume	42
Issue number	1
DOIs	https://doi.org/10.3892/ijo.2012.1700
State	Published - Jan 2013

Keywords

Cell migration
Mesenchymal stem cells
Phosphoinositide-3 kinase/protein kinase B pathway
Protein kinase B Inhibitors
Wound healing

ASJC Scopus subject areas

Oncology
Cancer Research

Access to Document

10.3892/ijo.2012.1700

Cite this

@article{124813c99c2b4e009c1d1c43dff2bf4f,

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.",

keywords = "Cell migration, Mesenchymal stem cells, Phosphoinositide-3 kinase/protein kinase B pathway, Protein kinase B Inhibitors, Wound healing",

author = "Zrinka Bulj and Serena Duchi and Alessandro Bevilacqua and Alessandro Gherardi and Barbara Dozza and Filippo Piccinini and Mariani, {Giulia Adalgisa} and Enrico Lucarelli and Sandro Giannini and Davide Donati and Sandra Marmiroli",

year = "2013",

month = jan,

doi = "10.3892/ijo.2012.1700",

language = "English (US)",

volume = "42",

pages = "118--126",

journal = "International Journal of Oncology",

issn = "1019-6439",

publisher = "Spandidos Publications",

number = "1",

}

TY - JOUR

T1 - Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells

AU - Bulj, Zrinka

AU - Duchi, Serena

AU - Bevilacqua, Alessandro

AU - Gherardi, Alessandro

AU - Dozza, Barbara

AU - Piccinini, Filippo

AU - Mariani, Giulia Adalgisa

AU - Lucarelli, Enrico

AU - Giannini, Sandro

AU - Donati, Davide

AU - Marmiroli, Sandra

PY - 2013/1

Y1 - 2013/1

N2 - 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.

AB - 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.

KW - Cell migration

KW - Mesenchymal stem cells

KW - Phosphoinositide-3 kinase/protein kinase B pathway

KW - Protein kinase B Inhibitors

KW - Wound healing

UR - http://www.scopus.com/inward/record.url?scp=84873657307&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84873657307&partnerID=8YFLogxK

U2 - 10.3892/ijo.2012.1700

DO - 10.3892/ijo.2012.1700

M3 - Article

C2 - 23165443

AN - SCOPUS:84873657307

VL - 42

SP - 118

EP - 126

JO - International Journal of Oncology

JF - International Journal of Oncology

SN - 1019-6439

IS - 1

ER -

Protein kinase B/AKT isoform 2 drives migration of human mesenchymal stem cells

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this