Functional and molecular adaptations in skeletal muscle of myoglobin-mutant mice
| Autor: | Annette Meeson, Kim S. Lau, Daniel J. Garry, Robert W. Grange, E. V A Chin, John M. Shelton, James T. Stull, R. Sanders Williams |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Genetically modified mouse
Hemeprotein Physiology Muscle Fibers Skeletal Mutant Oxidative phosphorylation Biology Extensor digitorum longus muscle Mice chemistry.chemical_compound Image Processing Computer-Assisted medicine Animals Muscle Skeletal Cyclic GMP In Situ Hybridization DNA Primers Mice Knockout Soleus muscle Myoglobin Reverse Transcriptase Polymerase Chain Reaction Skeletal muscle Cell Biology Adaptation Physiological medicine.anatomical_structure Biochemistry chemistry Regional Blood Flow Mutation Muscle Contraction |
| Zdroj: | American Journal of Physiology-Cell Physiology. 281:C1487-C1494 |
| ISSN: | 1522-1563 0363-6143 |
| DOI: | 10.1152/ajpcell.2001.281.5.c1487 |
| Popis: | Myoglobin is a cytoplasmic hemoprotein that is restricted to cardiomyocytes and oxidative skeletal myofibers and facilitates oxygen delivery during periods of high metabolic demand. Myoglobin content in skeletal muscle increases in response to hypoxic conditions. However, we previously reported that myoglobin-null mice are viable and fertile. In the present study, we define important functional, cellular, and molecular compensatory adaptations in the absence of myoglobin. Mice without myoglobin manifest adaptations in skeletal muscle that include a fiber type transition (type I to type II in the soleus muscle), increased expression of the hypoxia-inducible transcription factors hypoxia-inducible factor (HIF)-1α and HIF-2 (endothelial PAS domain protein), stress proteins such as heat shock protein 27, and the angiogenic growth factor vascular endothelial growth factor (soleus muscle), as well as increased nitric oxide metabolism (extensor digitorum longus). The resulting changes in angiogenesis, nitric oxide metabolism, and vasomotor regulation are likely to account for preserved exercise capacity of animals lacking myoglobin. These results demonstrate that mammalian organisms are capable of a broad spectrum of adaptive responses that can compensate for a potentially serious defect in cellular oxygen transport. |
| Databáze: | OpenAIRE |
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