Abstract
We studied the role of intracellular signal molecules PI3K, MAPK ERK1/2, and p38 in the realization of the growth potential of mesenchymal progenitor elements. Under in vitro conditions, PI3K и ERK1/2 specifi c inhibitors reduced fi broblastic colony- and cluster-formation and considerably suppressed proliferative activity of mesenchymal precursors. Blocker of p38 and protein kinase B had no effect on the function of fi broblast CFU.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Cell Culture Techniques
-
Cell Proliferation
-
Cells, Cultured
-
Chromones / pharmacology
-
Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
-
Extracellular Signal-Regulated MAP Kinases / metabolism*
-
MAP Kinase Signaling System
-
Mesenchymal Stem Cells / drug effects
-
Mesenchymal Stem Cells / physiology*
-
Mice, Inbred C57BL
-
Morpholines / pharmacology
-
Phosphatidylinositol 3-Kinases / metabolism*
-
Phosphoinositide-3 Kinase Inhibitors
-
Protein Kinase Inhibitors / pharmacology
-
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
-
p38 Mitogen-Activated Protein Kinases / metabolism*
Substances
-
Chromones
-
Morpholines
-
Phosphoinositide-3 Kinase Inhibitors
-
Protein Kinase Inhibitors
-
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
-
Extracellular Signal-Regulated MAP Kinases
-
p38 Mitogen-Activated Protein Kinases