Cholesterol depletion by methyl-?-cyclodextrin enhances myoblast fusion and induces the formation of myotubes with disorganized nuclei

Mermelstein, Cláudia; Portilho, Débora M.; Medeiros, Rommel B.; Matos, Aline da Rocha; Einicker‐Lamas, Marcelo; Tortelote, Giovane G.; Vieyra, Adalberto; Costa, Márcio Henrique Sá Netto

doi:10.1007/s00441-004-1004-5

Cited by 33 publications

(50 citation statements)

References 25 publications

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“…We could show in primary chick myogenic cultures that, upon treatment with the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate, desmin is phosphorylated, the myofibrils disassemble but the IF network persists, and the nuclei are clustered together in the center (57). Our recent results show that cholesterol withdrawal with the drug methylbeta-cyclodextrin also induces nucleus misalignment (58).…”

Section: Putative Functionsmentioning

confidence: 87%

Desmin: molecular interactions and putative functions of the muscle intermediate filament protein

Costa

Escaleira

Cataldo

et al. 2004

Braz J Med Biol Res

115

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Desmin is the intermediate filament (IF) protein occurring exclusively in muscle and endothelial cells. There are other IF proteins in muscle such as nestin, peripherin, and vimentin, besides the ubiquitous lamins, but they are not unique to muscle. Desmin was purified in 1977, the desmin gene was characterized in 1989, and knock-out animals were generated in 1996. Several isoforms have been described. Desmin IFs are present throughout smooth, cardiac and skeletal muscle cells, but can be more concentrated in some particular structures, such as dense bodies, around the nuclei, around the Z-line or in costameres. Desmin is up-regulated in muscle-derived cellular adaptations, including conductive fibers in the heart, electric organs, some myopathies, and experimental treatments with drugs that induce muscle degeneration, like phorbol esters. Many molecules have been reported to associate with desmin, such as other IF proteins (including members of the membrane dystroglycan complex), nebulin, the actin and tubulin binding protein plectin, the molecular motor dynein, the gene regulatory protein MyoD, DNA, the chaperone αB-crystallin, and proteases such as calpain and caspase. Desmin has an important medical role, since it is used as a marker of tumors' origin. More recently, several myopathies have been described, with accumulation of desmin deposits. Yet, after almost 30 years since its identification, the function of desmin is still unclear. Suggested functions include myofibrillogenesis, mechanical support for the muscle, mitochondrial localization, gene expression regulation, and intracellular signaling. This review focuses on the biochemical interactions of desmin, with a discussion of its putative functions.

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Section: Putative Functionsmentioning

confidence: 87%

Desmin: molecular interactions and putative functions of the muscle intermediate filament protein

Costa

Escaleira

Cataldo

et al. 2004

Braz J Med Biol Res

115

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“…We used the substance methyl-betacyclodextrin (MbCD) as a tool to selectively remove cholesterol molecules from the plasma membrane of chick skeletal muscle cells grown in culture. Our results showed that cholesterol depletion by MbCD induces the proliferation of myoblasts [22], increases myoblast fusion and lead to the formation of myotubes with increased size [15]. Furthermore, we showed that the Wnt/beta-catenin pathway is activated by cholesterol depletion [17,22].…”

mentioning

confidence: 54%

“…These cultures contain at least 80% myoblasts [15]. These myoblasts then proliferate, migrate and align with other myoblasts to fuse and form long multinucleated myotubes, which are clearly visible in 48-h cultures.…”

Section: Resultsmentioning

confidence: 96%

Knockdown of Lmo7 inhibits chick myogenesis

et al. 2016

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Edited by Dietmar MansteinThe multifunctional protein Lmo7 has been implicated in some aspects of myogenesis in mammals. Here we studied the distribution and expression of Lmo7 and the effects of Lmo7 knockdown in primary cultures of chick skeletal muscle cells. Lmo7 was localized within the nuclei of myoblasts and at the perinuclear region of myotubes. Knockdown of Lmo7 using siRNA specific to chick reduces the number and width of myotubes and the number of MyoD positive-myoblasts. Both Wnt3a enriched medium and Bio, activators of the Wnt/beta-catenin pathway, could rescue the effects of the Lmo7 knockdown suggesting a crosstalk between the Wnt/beta-catenin and Lmo7-mediated signaling pathways. Our data shows a role of Lmo7 during the initial events of chick skeletal myogenesis, particularly in myoblast survival.

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“…Muscle cells -Primary cultures of myogenic cells were prepared from the breast muscles of 11-day-old chick embryos as previously described (Mermelstein et al 2005). The L6 skeletal muscle cell line was obtained from BCRJ and maintained in DMEM supplemented with 10% FBS.…”

Section: Trichomonas Vaginalis Andmentioning

confidence: 99%

Trichomonas vaginalis and Tritrichomonas foetus: interaction with fibroblasts and muscle cells - new insights into parasite-mediated host cell cytotoxicity

Vilela

Benchimol

2012

Mem. Inst. Oswaldo Cruz

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Trichomonas vaginalis and Tritrichomonas foetus are parasitic, flagellated protists that inhabit the urogenital tract of humans and bovines, respectively. T. vaginalis causes the most prevalent non-viral sexually transmitted disease worldwide and has been associated with an increased risk for human immunodeficiency virus-1 infection in humans. Infections by T. foetus cause significant losses to the beef industry worldwide due to infertility and spontaneous abortion in cows. Several studies have shown a close association between trichomonads and the epithelium of the urogenital tract. However, little is known concerning the interaction of trichomonads with cells from deeper tissues, such as fibroblasts and muscle cells. Published parasite-host cell interaction studies have reported contradictory results regarding the ability of T. foetus and T. vaginalis to interact with and damage cells of different tissues. In this study, parasite-host cell interactions were examined by culturing primary human fibroblasts obtained from abdominal biopsies performed during plastic surgeries with trichomonads. In addition, mouse 3T3 fibroblasts, primary chick embryo myogenic cells and L6 muscle cells were also used as models of target cells. The parasite-host cell cultures were processed for scanning and transmission electron microscopy and were tested for cell viability and cell death. JC-1 staining, which measures mitochondrial membrane potential, was used to determine whether the parasites induced target cell damage. Terminal deoxynucleotidyltransferase-mediated dUTP nick end labelling staining was used as an indicator of chromatin damage. The colorimetric crystal violet assay was performed to ana-lyse the cytotoxicity induced by the parasite. The results showed that T. foetus and T. vaginalis adhered to and were cytotoxic to both fibroblasts and muscle cells, indicating that trichomonas infection of the connective and muscle tissues is likely to occur; such infections could cause serious risks to the infected host

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Cholesterol depletion by methyl-?-cyclodextrin enhances myoblast fusion and induces the formation of myotubes with disorganized nuclei

Cited by 33 publications

References 25 publications

Desmin: molecular interactions and putative functions of the muscle intermediate filament protein

Desmin: molecular interactions and putative functions of the muscle intermediate filament protein

Knockdown of Lmo7 inhibits chick myogenesis

Trichomonas vaginalis and Tritrichomonas foetus: interaction with fibroblasts and muscle cells - new insights into parasite-mediated host cell cytotoxicity

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