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Stem cell factor and H 2 O 2 induce GLUT1 translocation in M07e cells
Author(s) -
Maraldi Tullia,
Fiorentini Diana,
Prata Cecilia,
Landi Laura,
Hakim Gabriele
Publication year - 2004
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520200204
Subject(s) - glut1 , tyrosine phosphorylation , glucose transporter , microbiology and biotechnology , protein tyrosine phosphatase , tyrosine kinase , phosphorylation , chemistry , kinase , intracellular , receptor tyrosine kinase , chromosomal translocation , stem cell factor , biochemistry , signal transduction , biology , stem cell , haematopoiesis , endocrinology , gene , insulin
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 H 2 O 2 . SCF and H 2 O 2 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 H 2 O 2 . 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 H 2 O 2 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) H 2 O 2 could act increasing the level of tyrosine phosphorylation through the inhibition of tyrosine phosphatases and mimicking the regulation role of endogenous ROS.