1,721,161 research outputs found
From Ejtm (European Journal of Translational Myology) to Ejt3M (European Journal of Translational Myology, Mobility, Medicine)
Full text linkThis first 2018 issue of the European Journal of Translational Myology presents many novelties, that demonstrate that the journal is vital and expanding its authorship, readership and relevance from focused fields of biology, physiology, diagnostic, management and rehabilitation of skeletal muscle tissue to the interesting and clinically relevant fields of human mobility and to those of general medicine. The Editorial Board is consequently being expanded to allow fair and expert evaluation of the broader interests and expertise of the Authors submitting manuscripts. Furthermore, we are considering the option to change the title of the journal from Ejtm to Ejt3M (Myology, Mobility, Medicine). Criticisms and suggestions are welcome
Will exercise mimetics hold promise?
Full text linkSkeletal muscle has long been known as the target of several growth factors and hormones, including IGFs, steroids, thyroid and neurohypophyseal hormones, often regulating both muscle development and homeostasis in postnatal life, as summarized in classical as well as more recent reviews [1-4]. Such a complex hormonal regulation is not surprising, if one considers the many diverse functions muscle exerts: mechanical force production, body temperature regulation and metabolic storage due to its protein content. Active muscle accounts for over 90% of total body energy expenditure. Much more recent is the view of muscle as the source of several hormones [5-7] making skeletal muscle the largest endocrine gland of the organism and probably the most complex, due to the number (hundreds) of peptides constituting its secretome
Highlights on Cachexia, from the 4th Cachexia Conference, Tampa (FL), 6-9 Dec 2007
No full textCachexia is a syndrome associated with many chronic diseases and is an independent risk
factor for mortality. Yet it is only in these last years that cachexia has received increasing
attention, as the recently instituted international congress on this topic indicates. Here we
review some of the most noteworthy contributions presented at the 4th Cachexia
Conference in December 2007. Of particular relevance is the fact that an official definition
of cachexia was at last formulated. The definition of cachexia, as well as of its diagnostic
criteria, will help both the clinical management of and basic research on this complex,
multi-factorial syndrome
Molecular mechanisms regulating skeletal muscle homeostasis: effects of V1a AVP receptor over-expression
Full text linkThe maintenance of a working skeletal musculature is conferred by its capacity to regenerate after mechanical or pathological injury. Most muscle pathologies are characterized by the progressive loss of muscle tissue due to chronic degeneration combined with the inability of the regeneration machinery to replace damaged myofibers. Cachexia or muscle wasting is characterized by a loss of adipose and muscle mass associated with a compromised muscle regenerative ability. Arg-vasopressin (AVP) is a potent myogenesis promoting factor and activates both the calcineurin and CaMK pathways, whose combined activation leads to the formation of transcription factor complexes in vitro. The local over-expression of V1a AVP receptor (V1aR) in injured muscle results in enhanced regeneration. V1aR over-expressing muscle exhibits early activation of satellite cells and regeneration markers and accelerated differentiation. Here we investigated the role of V1aR over-expression in animals undergoing cachexia as a result of muscle over-expression of a specific cytokine (TNF). In these conditions, the local V1aR over-expression counteracts the negative effects of cachexia on muscle, as demonstrated by morphological and biochemical analysis. In particular, the presence of V1aR results in increased Pax-7, myogenin and myosin expression levels both in wild type and in cachectic muscles. The positive effects of V1aR on muscle homeostasis are due to the promotion of the calcineurin-IL-4 pathway and to the inhibition of atrophic genes expression mediated by FOXO phosphorylation. This study highlights a novel in vivo role for the AVP-dependent pathways which may suggest a potential gene therapy approach for many diseases affecting muscle homeostasis
Phosphorylation of specific polypeptides induced by 12-O-tetradecanoylphorbol-13-acetate in chick embryo fibroblasts.
No full textThe tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces, in cultured chick embryo fibroblasts, a generalised increase of the incorporation of labelled inorganic phosphate, and stimulates the phosphorylation of at least two polypeptide bands, 26 K and 65 K. Stimulation of the phosphorylation of 26 K and 65 K occurs within minutes of the addition of TPA to the culture medium of chick embryo fibroblasts, but it can also be evidenced at later times. Removal of TPA from the culture medium causes reversion of this effect. Stimulation of the phosphorylation of 26 K is also induced by the Ca2+-ionophore A23187, but the calmodulin inhibitor trifluoperazine does not inhibit the TPA induced stimulation of polypeptide phosphorylation. Agents increasing the intracellular cAMP concentration do not stimulate the phosphorylation of 26 K and 65 K. The results obtained suggest that the phosphorylation of specific polypeptides, probably induced by TPA through a Ca2+-phospholipid dependent mechanism, may represent an early regulative event which may be relevant for the pleiotropic effect of TPA in cultured normal cells
Bimodal effects of TNF-alpha on differentiation and hypertrophy of skeletal muscle cell cultures
No full textIn order to investigate the mechanisms regulating skeletal muscle homeostasis and the balance between atrophic and hypertrophic signals, and based on the fact that often factors with a positive (or negative) role in in vitro myogenesis have the same role in muscle homeostasis in vivo, we have exposed muscle cell cultures to Tumor Necrosis Factor-α (TNF-α), Insulin-like Growth Factor I (IGF-I) or their combination in two different experimental sets: L6 myogenic cells were induced to differentiate either in the absence or presence of these factors; alternatively, the same cells were differentiated with standard methods (by lowering the serum concentration) and then exposed to the above factors. With this approach we could confirm that TNF-α and IGF-I have opposite effects on skeletal muscle differentiation. However, we showed that both TNF-α and IGF-I induce muscle hypertrophy to the same extent when delivered to a promiscuous culture of myotubes and single cells. This striking observation may contribute to explain why muscle hypertrophy often involves muscle damage (and a consequent cytokine-mediated cycle of inflamma-tion). On the other hand, we extended previous observations on IGF-I hypertrophic effects on skeletal muscle cell obtained by using transgenic cell lines: here we show that IGF-I retains its ability to positively affect myogenesis even on cell cultures which have already reached a significant fusion index. Taken together our observations indicate that TNF-α has differential effects on myogenic differentiation and trophysm depending on the time it has been added to the cell culture. Both TNF-α and IGF-I can promote significantly myotube growth when added to muscle cell culture previously induced to differentiate
Calcium-, phospholipid-dependent protein kinase activity of cultured rat Sertoli cells and its modifications by vitamin A
No full textThe activity of the calcium-, phospholipid-dependent protein kinase (PKc) was partially characterized in Sertoli cell cultures prepared from 20-day-old rats. The calcium dependency, the requirements for phosphatidylserine and diolein, as well as the Km for ATP and for the tumor promoter TPA, were determined in total cell extracts. The specific activity of PKc was almost 3-fold higher in the soluble than in the particulate fraction of Sertoli cells. Treatment of cultured Sertoli cells with retinol inhibited, within 1 h of treatment, both the soluble and the particulate fraction-associated PKc activity, with an IC50 of 0.1 microM. Partial inhibition of PKc activity was obtained treating Sertoli cell cultures with FSH, while testosterone was ineffective. However, both FSH and testosterone potentiated the inhibitory effect of retinol. Less differentiated Sertoli cells, obtained from 8-day-old rats, displayed higher PKc activity and a pattern of subcellular distribution of the enzyme opposite to that of Sertoli cells obtained from 20-day-old rats. These data suggest that the actual PKc activity of rat Sertoli cells be negatively regulated by retinol and, spontaneously, during the progression of Sertoli cell differentiation
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