Publications by authors named "Irina V Kravchenko"

Objective: Insulin-like growth factor I (IGF1) is an important regulator of collagen and extracellular matrix protein expression. We aimed to evaluate the effect of amino acids (AAs) on expression of IGF1 and IGF1-dependent genes in human myotubes and skeletal muscle and supposed that AAs administration increases IGF1 levels in blood and expression of IGF1 and IGF1-dependent genes in trained skeletal muscle, thereby reducing training-induced muscle damage.

Design: Human myotubes were incubated with Arg and Leu for 24 h.

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The effects of glycated albumin on the expression of inflammatory cytokines in differentiated myotubes were investigated. Glycated albumin stimulates the expression of TNF α, IL-1β, IL-6 and CCL-2 both at the mRNA and protein levels via the receptor of AGEs. Various cytokines demonstrated different kinetics of stimulation by glycated albumin.

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The effects of potassium chloride on the expression of IGF-1 splice forms and myoblast proliferation were investigated. KCl at the concentrations of 7-12 mM stimulated the synthesis of IGF-1 and mechano growth factor (MGF) in murine myoblasts as well as in myotubes both at the mRNA and protein levels. Pan-calcium channel blocker CdCl completely abolished stimulation of growth factor expression, whereas blocker of HCN and Na1.

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Myofibrillar proteins titin and myomesin stimulated myoblast proliferation as determined by MTT-test and labelled thymidine incorporation in the DNA. Specific Fn type III and Ig-like domains of these proteins were able to exert mitogenic effects as well. Proliferative effect of Fn type III domains was highly sensitive to inhibition of Ca/calmodulin dependent protein kinase, whereas the effect of Ig-like domains showed greater sensitivity to the inhibition of adenylyl cyclase - cAMP - PKA pathway.

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Expression of insulin-like growth factor 1 (IGF-1) mRNAs splice forms was recently shown to be stimulated by myofibrillar proteins released from the damaged muscle. In this study, we report that individual subfragments of titin and myomesin composed of Fn type III and Ig-like domains can activate expression of two IGF-1 splice forms in cultured myoblasts, both at protein and mRNA levels. Competition studies showed that each of the domain-types interacts with its own receptor.

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Introduction: We investigated the effect of resistance exercise intensity and exercise-induced metabolic stress on the activation of anabolic signaling and expression of myogenic genes in skeletal muscle.

Methods: Ten strength-trained athletes performed high-intensity [HI, 74% of 1-repetition maximum (RM)], middle-intensity (MI, 54% 1RM), or middle-intensity (54% 1RM) no-relaxation exercise (MIR). Kinase phosphorylation level and myogenic gene expression in muscle samples were evaluated before, 45 min, 5 h, and 20 h after exercise.

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Mechano-growth factor (MGF) is a product of alternative splicing of the insulin-like growth factor 1 (IGF-1) mRNA. MGF is known to stimulate myoblast proliferation and to protect neurons and cardiomyocytes from apoptosis. MGF expression is dramatically increased in response to mechanical stimuli and tissue damage.

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The effect of second messengers on the expression of mechano-growth factor (MGF) synthesis by myoblasts and differentiated myotubes in culture was investigated. cAMP stimulates MGF expression both in murine and human cells. CNG- and HCN-channel blockers slightly activated MGF synthesis, while an activator of Epac protein had no effect.

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The effect of cellular stress factors, the hyperthermia and the acidification of culture medium, on mechano-growth factor (MGF) synthesis by murine myoblasts in culture was investigated. Hyperthermia was shown to stimulate MGF expression both in primary myoblasts and in differentiated multinuclear myotubes. The induction of MGF synthesis peaked at 40 degrees capital ES, Cyrillic, with some activation at 39 and 41 degrees capital ES, Cyrillic.

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Two hybridoma clones secreting monoclonal antibodies (MAbs) to mechano-growth factor (MGF) have been produced by cell fusion technique. Isotyping of the MAbs revealed that both belong to the G1 subclass. The epitope specificity of the MAbs has been examined in competition experiments.

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Exposure to asbestos fibers increases the risk of development of mesotheliomas and lung carcinomas, but not fibrosarcomas. We present data suggesting that resistance of fibroblasts to asbestos-induced carcinogenesis is likely to be connected with their lower ability to generate reactive oxygen species (ROS) in response to asbestos exposure and stricter control of proliferation of cells bearing asbestos/ROS-induced injuries. In fact, chrysotile (Mg6Si4O10(OH)8) asbestos exposure (5-10 microg/cm2) increased intracellular ROS and 8-oxo-guanine contents in rat pleural mesothelial cells, but not in lung fibroblasts.

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The report is devoted to the investigation of cytotoxic action of macrophages and asbestos on transformed mesothelium and mesothelioma cells, the characterization of its specificity, and the nature of the factors mediating it. The viability of different cells after asbestos exposure was studied in co-culture with macrophages. Mesothelioma cell lines obtained from tumors developed in vivo were the most sensitive to the cytotoxic action of macrophages and asbestos.

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