title: Contribution of the PI3K/Akt/PKB signal pathway to maintenance of self-renewal in human embryonic stem cells.
abstract: Although basic fibroblast growth factor (FGF2) is generally included in the media for maintenance of human embryonic stem cells (hESCs), the action of FGF2 in these cells has not been well defined. Here, we determined the roles of FGF2 in maintaining hESC self-renewal. Withdrawal of FGF2 from the media led to acquisition of typical differentiated characteristics in hESCs. In the presence of FGF2, which is normally required for proliferation in an undifferentiated state, inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt/PKB signal stimulated differentiation and attenuated the expression of extracellular matrix (ECM) molecules. We suggest that FGF2 maintains hESC self-renewal by supporting stable expression of ECM molecules through activation of the PI3K/Akt/PKB pathway.
authors.affiliation: Division of Stem Cell Biology, Medical Research Center, MizMedi Hospital, 701-4 Naebalsandong, Kangseogu, Seoul 157-280, South Korea.
authors.forename: Sun Jong
authors.initials: SJ
authors.lastname: Kim
authors.forename: Seon Hye
authors.initials: SH
authors.lastname: Cheon
authors.forename: Seung Jun
authors.initials: SJ
authors.lastname: Yoo
authors.forename: Jinie
authors.initials: J
authors.lastname: Kwon
authors.forename: Jong Hyuk
authors.initials: JH
authors.lastname: Park
authors.forename: Chul Geun
authors.initials: CG
authors.lastname: Kim
authors.forename: Kunsoo
authors.initials: K
authors.lastname: Rhee
authors.forename: Seungkwon
authors.initials: S
authors.lastname: You
authors.forename: Joo-Yong
authors.initials: JY
authors.lastname: Lee
authors.forename: Sung Il
authors.initials: SI
authors.lastname: Roh
authors.forename: Hyun Soo
authors.initials: HS
authors.lastname: Yoon
mesh_terms: D064413:3-Phosphoinositide-Dependent Protein Kinases; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D002867:Chromones / Q000494:pharmacology; D004622:Embryo, Mammalian / Q000166:cytology*; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D009025:Morpholines / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000502:physiology; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt; D017474:Receptors, Laminin / Q000502:physiology; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology / Q000187:drug effects / Q000201:enzymology*
chemical_list: D064413:3-Phosphoinositide-Dependent Protein Kinases; D002867:Chromones; D016326:Extracellular Matrix Proteins; D016222:Fibroblast Growth Factor 2; D009025:Morpholines; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D051057:Proto-Oncogene Proteins c-akt; D017474:Receptors, Laminin; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; C494918:AKT1 protein, human