Endothelial nitric oxide synthase is involved in calcium-induced Akt signaling in mouse skeletal muscle
Autor: | Vitor A. Lira, Dana L. Brown, Quinlyn A. Soltow, Jason A. Drenning, Claire N. Canon, David S. Criswell, Lauren M. Valera |
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Rok vydání: | 2009 |
Předmět: |
Male
Cancer Research medicine.medical_specialty Nitric Oxide Synthase Type III Physiology Clinical Biochemistry Muscle Fibers Skeletal Nitric Oxide Biochemistry Nitric oxide chemistry.chemical_compound Mice Enos Internal medicine medicine Animals Phosphorylation Muscle Skeletal Protein kinase B Cyclic GMP PI3K/AKT/mTOR pathway Cells Cultured biology Myosin Heavy Chains Myogenesis Skeletal muscle biology.organism_classification Mice Mutant Strains Endocrinology medicine.anatomical_structure chemistry Mutation Calcium Proto-Oncogene Proteins c-akt Signal Transduction |
Zdroj: | Nitric oxide : biology and chemistry. 21(3-4) |
ISSN: | 1089-8611 |
Popis: | We hypothesized that targeted mutation of the endothelial nitric oxide synthase (eNOS) gene would reduce Akt-related signaling events in skeletal muscle cells, compared to wild type (WT) controls. Results show that slow myosin heavy chain (type I/beta) expression and the abundance of slow-twitch fibers are reduced in plantaris muscle of eNOS(-/-) mice, compared to WT. Further, basal phosphorylation of Akt (p-Akt (Ser-473)/total Akt) and GSK-3beta (GSK-3beta (Ser-9)/total GSK-3beta) are reduced 60-70% in primary myotubes from eNOS(-/-) mice. Treatment with the calcium ionophore, A23187 (0.4 microM, 1 h), increased phosphorylation of Akt and GSK-3beta by approximately 2-fold (P |
Databáze: | OpenAIRE |
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