RhoA controls myoblast survival by inducing the phosphatidylinositol 3-kinase-Akt signaling pathway

The small GTPase RhoA regulates the expression of the myogenic transcription factor, MyoD, and the transcription of muscle-specific genes. We report that RhoA also affects the survival of differentiating myoblasts. Two signaling pathways, extracellular signal-regulated kinase (ERK) and phosphatidyli...

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Bibliographic Details
Published in:FEBS letters 2004-07, Vol.569 (1-3), p.129-134
Main Authors: Reuveny, Mickol, Heller, Hanna, Bengal, Eyal
Format: Article
Language:English
Subjects:
Act, activated
Animals
Apoptosis
Cell Differentiation
Cell Line
Cell Survival
Clone Cells
DM, differentiation medium
DN, dominant negative
Enzyme Induction
ERK, extracellular signal-regulated kinase
GM, growth medium
MD:ER, MyoD-estrogen receptor
MHC, myosin heavy chain
Muscle differentiation
Myoblasts - cytology
Phosphatidylinositol 3-Kinases - metabolism
PI3-K, phosphatidylinositol 3-kinase
PI3-K-Akt signaling pathway
Protein-Serine-Threonine Kinases - metabolism
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-akt
Recombinant Proteins - metabolism
Rho GTPase
rhoA GTP-Binding Protein - metabolism
ROK, Rho kinase
Signal Transduction
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Summary:The small GTPase RhoA regulates the expression of the myogenic transcription factor, MyoD, and the transcription of muscle-specific genes. We report that RhoA also affects the survival of differentiating myoblasts. Two signaling pathways, extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3-K)-Akt, are involved in myoblast survival. Here, we show that inhibition of RhoA prevents the phosphorylation of Akt, but does not affect the phosphorylation of ERK. Constitutive expression of an active form of Akt prevents apoptosis in myoblasts treated with the Rho inhibitor C3-transferase. These results indicate that RhoA functions to prevent myoblast death by inducing the PI3-K-Akt pathway.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2004.05.035