Stem cell factor and H2O2 induce GLUT1 translocation in M07e cells.
This work aims to elucidate the mechanisms involved in the early activation of glucose transport in hematopoietic M07e cells by stem cell factor (SCF) and a reactive oxygen species (ROS) as H2O2. SCF and H2O2 increase Vmax for glucose transport; this enhancement is due to a higher content in GLUT1 in plasma membranes, possibly through a translocation from intracellular stores. Inhibitors of tyrosine kinases or phospholipase C (PLC) remove glucose transport enhancement and prevent translocation. The inhibitory effect of STI-571 suggests a role for c-kit tyrosine kinase on glucose transport activation not only by SCF, but also by H2O2. On the other hand, neither protein kinase C nor phosphoinositide-3-kinase appear to be involved in the acute activation of glucose transport. Our data suggest that i) in M07e cells, SCF and exogenous H2O2 elicit a short-term activation of glucose transport through a translocation of GLUT1 from intracellular stores to plasma membranes; ii) both stimuli could share at least some signaling pathways leading to glucose uptake activation, involving protein tyrosine kinases and PLC iii) H2O2 could act increasing the level of tyrosine phosphorylation through the inhibition of tyrosine phosphatases and mimicking the regulation role of endogenous ROS.
Dipartimento di Biochimica G. Moruzzi, Università di Bologna, Via Irnerio 48, I-40126 Bologna, Italy.
Tullia
T
Maraldi
Diana
D
Fiorentini
Cecilia
C
Prata
Laura
L
Landi
Gabriele
G
Hakim
D001692:Biological Transport / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D051272:Glucose Transporter Type 1; D006412:Hematopoietic Stem Cells / Q000378:metabolism*; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D007700:Kinetics; D007938:Leukemia; D008533:Megakaryocytes; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000037:antagonists & inhibitors; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000502:physiology; D017382:Reactive Oxygen Species / Q000494:pharmacology; D015398:Signal Transduction; D019089:Stem Cell Factor / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000502:physiology; D014443:Tyrosine / Q000378:metabolism
D004791:Enzyme Inhibitors; D005947:Glucose; D051272:Glucose Transporter Type 1; D006861:Hydrogen Peroxide; D009004:Monosaccharide Transport Proteins; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D011505:Protein-Tyrosine Kinases; D017382:Reactive Oxygen Species; D019089:Stem Cell Factor; D010738:Type C Phospholipases; D014443:Tyrosine; C495677:SLC2A1 protein, human