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Grb10 Deletion Enhances Muscle Cell Proliferation, Differentiation and GLUT4 Plasma Membrane Translocation
Journal of cellular physiology, 2014-11, Vol.229 (11), p.1753-1764
Mokbel, Nancy
Hoffman, Nolan J.
Girgis, Christian M.
Small, Lewin
Turner, Nigel
Daly, Roger J.
Cooney, Gregory J.
Holt, Lowenna J.
2014
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Mokbel, Nancy
Hoffman, Nolan J.
Girgis, Christian M.
Small, Lewin
Turner, Nigel
Daly, Roger J.
Cooney, Gregory J.
Holt, Lowenna J.
Titel
Grb10 Deletion Enhances Muscle Cell Proliferation, Differentiation and GLUT4 Plasma Membrane Translocation
Ist Teil von
Journal of cellular physiology, 2014-11, Vol.229 (11), p.1753-1764
Ort / Verlag
United States: Blackwell Publishing Ltd
Erscheinungsjahr
2014
Quelle
Wiley Online Library All Journals
Beschreibungen/Notizen
Grb10 is an intracellular adaptor protein which binds directly to several growth factor receptors, including those for insulin and insulin‐like growth factor receptor‐1 (IGF‐1), and negatively regulates their actions. Grb10‐ablated (Grb10‐/‐) mice exhibit improved whole body glucose homeostasis and an increase in muscle mass associated specifically with an increase in myofiber number. This suggests that Grb10 may act as a negative regulator of myogenesis. In this study, we investigated in vitro, the molecular mechanisms underlying the increase in muscle mass and the improved glucose metabolism. Primary muscle cells isolated from Grb10‐/‐ mice exhibited increased rates of proliferation and differentiation compared to primary cells isolated from wild‐type mice. The improved proliferation capacity was associated with an enhanced phosphorylation of Akt and ERK in the basal state and changes in the expression of key cell cycle progression markers involved in regulating transition of cells from the G1 to S phase (e.g., retinoblastoma (Rb) and p21). The absence of Grb10 also promoted a faster transition to a myogenin positive, differentiated state. Glucose uptake was higher in Grb10‐/‐ primary myotubes in the basal state and was associated with enhanced insulin signaling and an increase in GLUT4 translocation to the plasma membrane. These data demonstrate an important role for Grb10 as a link between muscle growth and metabolism with therapeutic implications for diseases, such as muscle wasting and type 2 diabetes. J. Cell. Physiol. 229: 1753–1764, 2014. © 2014 Wiley Periodicals, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0021-9541
eISSN: 1097-4652
DOI: 10.1002/jcp.24628
Titel-ID: cdi_proquest_journals_1548801673
Format
–
Schlagworte
Animals
,
Biomarkers - metabolism
,
CD56 Antigen - metabolism
,
Cell Cycle - drug effects
,
Cell Differentiation - drug effects
,
Cell Differentiation - genetics
,
Cell Membrane - drug effects
,
Cell Membrane - metabolism
,
Cell Proliferation - drug effects
,
Cell Separation
,
Cells, Cultured
,
Extracellular Signal-Regulated MAP Kinases - metabolism
,
Gene Deletion
,
Gene Expression Regulation - drug effects
,
Glucose - metabolism
,
GRB10 Adaptor Protein - genetics
,
GRB10 Adaptor Protein - metabolism
,
Insulin - pharmacology
,
MAP Kinase Signaling System - drug effects
,
Mice
,
Mice, Inbred C57BL
,
Muscle Cells - cytology
,
Muscle Cells - drug effects
,
Muscle Cells - metabolism
,
Muscle Fibers, Skeletal - metabolism
,
Myoblasts, Skeletal - cytology
,
Myoblasts, Skeletal - drug effects
,
Myoblasts, Skeletal - enzymology
,
Myogenin - metabolism
,
Protein Transport - drug effects
,
Proto-Oncogene Proteins c-akt - metabolism
,
RNA, Messenger - genetics
,
RNA, Messenger - metabolism
,
Satellite Cells, Skeletal Muscle - cytology
,
Satellite Cells, Skeletal Muscle - drug effects
,
Satellite Cells, Skeletal Muscle - metabolism
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