Vinculin and meta-vinculin in fast and slow rat skeletal muscle before and after hindlimb suspension

Chopard, Angèle; Pons, Françoise; Marini, Jean-François

doi:10.1007/s00424-002-0872-3

Cited by 16 publications

(28 citation statements)

References 37 publications

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“…In addition, ultrastructural studies have clearly shown that membrane folding and the length of the membrane interface between muscle fiber and tendon are largely increased after hindlimb suspension (91) and spaceflight (63), which might confirm the increase in collagen content in disuse situations. Our previous work conducted with muscle unloading (in both humans and animals) also reported structural changes affecting the expression of several cytoskeletal and associated proteins (22)(23)(24). Together, these results show that collagen and ECM components play a major role in remodeling of skeletal muscle during disuse-induced atrophy.…”

Section: Discussionmentioning

confidence: 57%

Large-scale mRNA analysis of female skeletal muscles during 60 days of bed rest with and without exercise or dietary protein supplementation as countermeasures

Chopard

LeCunff

Danger

et al. 2009

Physiological Genomics

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Chopard A, Lecunff M, Danger R, Lamirault G, Bihouee A, Teusan R, Jasmin BJ, Marini JF, Leger JJ. Large-scale mRNA analysis of female skeletal muscles during 60 days of bed rest with and without exercise or dietary protein supplementation as countermeasures. Physiol Genomics 38: 291-302, 2009. First published May 26, 2009 doi:10.1152/physiolgenomics.00036.2009.-Microgravity has a dramatic impact on human physiology, illustrated in particular, with skeletal muscle impairment. A thorough understanding of the mechanisms leading to loss of muscle mass and structural disorders is necessary for defining efficient clinical and spaceflight countermeasures. We investigated the effects of long-term bed rest on the transcriptome of soleus (SOL) and vastus lateralis (VL) muscles in healthy women (BRC group, n ϭ 8), and the potential beneficial impact of protein supplementation (BRN group, n ϭ 8) and of a combined resistance and aerobic training (BRE group, n ϭ 8). Gene expression profiles were obtained using a customized microarray containing 6,681 muscles-relevant genes. A two-class statistical analysis was applied on 2,103 genes with consolidated expression in BRC, BRN, and BRE groups. We identified 472 and 207 mRNAs whose expression was modified in SOL and VL from BRC group, respectively. Further clustering analysis, identifying relevant biological mechanisms and pathways, reported five main subclusters. Three are composed of upregulated mRNAs involved mainly in nucleic acid and protein metabolism, and two made up of downregulated transcripts encoding components involved in energy metabolism. Exercise countermeasure demonstrated drastic compensatory effects, decreasing the number of differentially expressed mRNAs by 89 and 96% in SOL and VL, respectively. In contrast, nutrition countermeasure had moderate effects and decreased the number of differentially-expressed transcripts by 40 and 25% in SOL and VL. Together, these data present a systematic, global and comprehensive view of the adaptive response of female muscle to long-term atrophy.skeletal muscle fiber; atrophy; microgravity; microarray; leucine SKELETAL MUSCLE IS ONE OF the most affected tissues in disuse situations since it can exhibit large structural and functional adaptations, depending on changes in the levels of imposed mechanical constraints (1). Neuromuscular activity is decreased by hypokinesia and hypodynamia, as well by microgravity environment resulting in skeletal muscle atrophy (35). Space exploration and interplanetary travel requires that humans be confronted with extended durations of space environment and weightlessness. From a few days in space (with the Mercury, Gemini, and Apollo-Soyouz programs), to several months in a space station (with Skylab, MIR, and the actual ISS), disuse-induced muscle atrophy and impairment is a biomedical challenge and a focus point of space sciences in studying the deleterious effects of microgravity (1,27,35).Human bed rest (BR), a ground-based model, provides an opportunity to understand the components of musc...

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Section: Discussionmentioning

confidence: 57%

Large-scale mRNA analysis of female skeletal muscles during 60 days of bed rest with and without exercise or dietary protein supplementation as countermeasures

Chopard

LeCunff

Danger

et al. 2009

Physiological Genomics

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“…Thus, it has been shown recently that a change in mechanical load in rat skeletal muscle results in increased metavinculin expression (50). Moreover, it is known that smooth muscle cells in culture down-regulate the expression of metavinculin very rapidly (51), possibly because of the lack of external stimuli, such as mechanical stretching.…”

Section: Discussionmentioning

confidence: 99%

Comparative Biochemical Analysis Suggests That Vinculin and Metavinculin Cooperate in Muscular Adhesion Sites

Witt

Zieseniß

Fock

et al. 2004

Journal of Biological Chemistry

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Metavinculin, the muscle-specific splice variant of the cell adhesion protein vinculin, is characterized by a 68-amino acid insert within the C-terminal tail domain. The findings that mutations within this region correlate with hereditary idiopathic dilated cardiomyopathy in man suggest a specific contribution of metavinculin to the molecular architecture of muscular actin-membrane attachment sites, the nature of which, however, is still unknown. In mice, metavinculin is expressed in smooth and skeletal muscle, where it co-localizes with vinculin in dense plaques and costameres, respectively, but is of conspicuously low abundance in the heart. Immunoprecipitates suggest that both isoforms are present in the same complex. On the molecular level, both vinculin isoforms are regulated via an intramolecular head-tail interaction, with the metavinculin tail domain having a lower affinity for the head as compared with the vinculin tail. In addition, metavinculin displays impaired binding to acidic phospholipids and reduced homodimerization. Only in the presence of phospholipidactivated vinculin tail, the metavinculin tail domain is readily incorporated into heterodimers. Mutational analysis revealed that the metavinculin insert significantly alters binding of the C-terminal hairpin loop to acidic phospholipids. In summary, our data lead to a model in which unfurling of the metavinculin tail domain is impaired by the negative charges of the 68-amino acid insert, thus requiring vinculin to fully activate the metavinculin molecule. As a consequence, microfilament anchorage may be modulated at muscular adhesion sites through heterodimer formation.

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“…The amount of metavinculin expressed in human cardiac tissue appears greater than that in mouse (84). Metavinculin levels can be increased by mechanical loading, as has been determined with rat skeletal muscle (15). Subcellularly, metavinculin and vinculin colocalize.…”

mentioning

confidence: 87%

Cardiac-Myocyte-Specific Excision of the Vinculin Gene Disrupts Cellular Junctions, Causing Sudden Death or Dilated Cardiomyopathy

Zemljic-Harpf

Miller

Henderson

et al. 2007

Molecular and Cellular Biology

184

206

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Vinculin is a ubiquitously expressed multiliganded protein that links the actin cytoskeleton to the cell membrane. In myocytes, it is localized in protein complexes which anchor the contractile apparatus to the sarcolemma. Its function in the myocardium remains poorly understood. Therefore, we developed a mouse model with cardiac-myocyte-specific inactivation of the vinculin (Vcl) gene by using Cre-loxP technology. Sudden death was found in 49% of the knockout (cVclKO) mice younger than 3 months of age despite preservation of contractile function. Conscious telemetry documented ventricular tachycardia as the cause of sudden death, while defective myocardial conduction was detected by optical mapping. cVclKO mice that survived through the vulnerable period of sudden death developed dilated cardiomyopathy and died before 6 months of age. Prior to the onset of cardiac dysfunction, ultrastructural analysis of cVclKO heart tissue showed abnormal adherens junctions with dissolution of the intercalated disc structure, expression of the junctional proteins cadherin and ␤1D integrin were reduced, and the gap junction protein connexin 43 was mislocalized to the lateral myocyte border. This is the first report of tissue-specific inactivation of the Vcl gene and shows that it is required for preservation of normal cell-cell and cell-matrix adhesive structures.

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Vinculin and meta-vinculin in fast and slow rat skeletal muscle before and after hindlimb suspension

Cited by 16 publications

References 37 publications

Large-scale mRNA analysis of female skeletal muscles during 60 days of bed rest with and without exercise or dietary protein supplementation as countermeasures

Large-scale mRNA analysis of female skeletal muscles during 60 days of bed rest with and without exercise or dietary protein supplementation as countermeasures

Comparative Biochemical Analysis Suggests That Vinculin and Metavinculin Cooperate in Muscular Adhesion Sites

Cardiac-Myocyte-Specific Excision of the Vinculin Gene Disrupts Cellular Junctions, Causing Sudden Death or Dilated Cardiomyopathy

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