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Involvement of eukaryotic translation initiation factor 5A (eIF5A) in skeletal muscle stem cell differentiation
Author(s) -
Luchessi Augusto D.,
Cambiaghi Tavane D.,
Hirabara Sandro M.,
Lambertucci Rafael H.,
Silveira Leonardo R.,
Baptista Igor L.,
Moriscot Anselmo S.,
CostaNeto Claudio M.,
Curi Rui
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21619
Subject(s) - skeletal muscle , spermidine , cellular differentiation , initiation factor , microbiology and biotechnology , biology , eukaryotic initiation factor , eukaryotic translation , translation (biology) , stem cell , protein biosynthesis , biochemistry , messenger rna , chemistry , gene , enzyme , endocrinology
The eukaryotic translation initiation factor 5A (eIF5A) contains a special amino acid residue named hypusine that is required for its activity, being produced by a post‐translational modification using spermidine as substrate. Stem cells from rat skeletal muscles (satellite cells) were submitted to differentiation and an increase of eIF5A gene expression was observed. Higher content of eIF5A protein was found in satellite cells on differentiation in comparison to non‐differentiated satellite cells and skeletal muscle. The treatment with N1‐guanyl‐1,7‐diaminoheptane (GC7), a hypusination inhibitor, reversibly abolished the differentiation process. In association with the differentiation blockage, an increase of glucose consumption and lactate production and a decrease of glucose and palmitic acid oxidation were observed. A reduction in cell proliferation and protein synthesis was also observed. L ‐Arginine, a spermidine precursor and partial suppressor of muscle dystrophic phenotype, partially abolished the GC7 inhibitory effect on satellite cell differentiation. These results reveal a new physiological role for eIF5A and contribute to elucidate the molecular mechanisms involved in muscle regeneration. J. Cell. Physiol. 218: 480–489, 2009. © 2008 Wiley‐Liss, Inc.