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1.

001-es BibID:BIBFORM049771
Első szerző:Bodnár Dóra (molekuláris biológus)
Cím:Hypermuscular mice with mutation in the myostatin gene display altered calcium signaling / Dóra Bodnár, Nikolett Geyer, Olga Ruzsnavszky, Tamás Oláh, Bence Hegyi, Mónika Sztretye, János Fodor, Beatrix Dienes, Ágnes Balogh, Zoltán Papp, László Szabó, Géza Müller, László Csernoch, Péter Szentesi
Dátum:2014
ISSN:0022-3751
Megjegyzések:Myostatin, a member of the transforming growth factor β family, is a potent negative regulator of skeletal muscle growth, as myostatin-deficient mice show a great increase in muscle mass. Yet the physical performance of these animals is reduced. As an explanation for this, alterations in the steps in excitation-contraction coupling were hypothesized and tested for in mice with the 12 bp deletion in the propeptide region of the myostatin precursor (MstnCmpt-dl1Abc or Cmpt). In voluntary wheel running, control C57BL/6 mice performed better than the mutant animals in both maximal speed and total distance covered. Despite the previously described lower specific force of Cmpt animals, the pCa-force relationship, determined on chemically permeabilized fibre segments, did not show any significant difference between the two mouse strains. While resting intracellular Ca2+ concentration ([Ca2+]i) measured on single intact flexor digitorum brevis (FDB) muscle fibres using Fura-2 AM was similar to control (72.0 ± 1.7 vs. 78.1 ± 2.9 nm, n = 38 and 45), the amplitude of KCl-evoked calcium transients was smaller (360 ± 49 vs. 222 ± 45 nm, n = 22) in the mutant strain. Similar results were obtained using tetanic stimulation and Rhod-2 AM, which gave calcium transients that were smaller (2.42 ± 0.11 vs. 2.06 ± 0.10 F/F0, n = 14 and 13, respectively) on Cmpt mice. Sarcoplasmic reticulum (SR) calcium release flux calculated from these transients showed a reduced peak (23.7 ± 3.0 vs. 15.8 ± 2.1 mMs-1) and steady level (5.7 ± 0.7 vs. 3.7 ± 0.5 mm s-1) with no change in the peak-to-steady ratio. The amplitude and spatial spread of calcium release events detected on permeabilized FDB fibres were also significantly smaller in mutant mice. These results suggest that reduced SR calcium release underlies the reduced muscle force in Cmpt animals.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
EC coupling
skeletal muscle
calcium release
myostatin
Molekuláris Medicina
Doktori iskola
Megjelenés:Journal of Physiology-London. - 592 : 6 (2014), p. 1353-1365. -
További szerzők:Geyer Nikolett Ruzsnavszky Olga (1983-) (élettanász) Oláh Tamás (1983-) (élettanász) Hegyi Bence (1987-) (élettanász) Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Fodor János (1973-) (élettanász, biotechnológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Balogh Ágnes (1984-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Szabó László Müller Géza Csernoch László (1961-) (élettanász) Szentesi Péter (1967-) (élettanász)
Pályázati támogatás:NN-107765
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A harántcsíkolt izom kontrakció molekuláris szabályozása
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
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DOI
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2.

001-es BibID:BIBFORM065772
Első szerző:Oláh Tamás (élettanász)
Cím:Cannabinoid signalling inhibits sarcoplasmic Ca2+ release and regulates excitation-contraction coupling in mammalian skeletal muscle / Tamás Oláh, Dóra Bodnár, Adrienn Tóth, János Vincze, János Fodor, Barbara Reischl, Adrienn Kovács, Olga Ruzsnavszky, Beatrix Dienes, Péter Szentesi, Oliver Friedrich, László Csernoch
Dátum:2016
ISSN:0022-3751
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Physiology-London 594 : 24 (2016), p. 7381-7398. -
További szerzők:Bodnár Dóra (1987-) (molekuláris biológus) Tóth Adrienn (1988-) (molekuláris biológus, élettanász) Vincze János (1947-) (biofizikus) Fodor János (1973-) (élettanász, biotechnológus) Reischl, Barbara Kovács Adrienn (1989-) (molekuláris biológus) Ruzsnavszky Olga (1983-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Szentesi Péter (1967-) (élettanász) Friedrich, Oliver Csernoch László (1961-) (élettanász)
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3.

001-es BibID:BIBFORM062408
Első szerző:Oláh Tamás (élettanász)
Cím:CB1 cannabinoid receptors are involved in the regulation of excitation-contraction coupling in mammalian skeletal muscle / Oláh Tamás, Bodnár Dóra, Tóth Adrienn, Fodor János, Kovács Adrienn, Farkas Anna, Nádró Bíborka, Szentesi Péter, Csernoch László
Dátum:2015
Megjegyzések:The presence of CB1 cannabinoid receptors (CB1R) has been shown in skeletal muscle, but it is yet to be cleared whether they have any significance in the regulation of contractions. CB1-knockout (CB1-KO) mice showed hypoactivity, however, it is questionable whether this was solely due to effects on the central nervous system or impairment of muscle function also contributes. Our aim was to investigate the role of CB1R in mammalian skeletal muscle, and the effects of cannabinoid drugs on Ca2+ transients. Running ability of control and CB1-KO mice was studied by activity-wheel-tests while in vivo muscle force of the animals was measured by grip-tests and hang-tests. Ca2+ transients evoked by KCl-depolarization in the presence and absence of cannabinoid agonists were investigated on flexor digitorum brevis (FDB) fibers of control and CB1-KO mice. CB1-KO mice performed worse as compared to control in all behavior tests applied. In contrast, depolarization-evoked Ca2+ transients were significantly higher in FDB fibers isolated from CB1-KO mice (848 ? 98 nM, n = 47) compared to control (376 ? 60 nM, n = 32, p\0.01). When KCl-evoked Ca2+ transients were repeated on control FDB fibers in the absence and presence of the CB1 agonist WIN55,212 (WIN), the transients after WIN treatment were significantly smaller (44 ? 7 % of the first transient, n = 27) than in untreated (79 ? 5 % of the first transient, n = 32, p\0.01) fibers. Our observations suggest that CB1R-mediated signaling contributes to the regulation of excitation?contraction coupling and skeletal muscle contractions. Nevertheless, the effects mediated by the absence of CB1R in the central nervous system on the inferior muscle performance of CB1-KO mice in vivo cannot be ruled out. These results can contribute to the identification of the side effects of medically used cannabinoid drugs on skeletal muscle.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Skeletal muscle
CB1 cannabinoid receptor
Excitation?contraction coupling
Megjelenés:Journal of muscle research and cell motility. - 36 (2015), p. 129. -
További szerzők:Bodnár Dóra (1987-) (molekuláris biológus) Tóth Adrienn (1988-) (molekuláris biológus, élettanász) Fodor János (1973-) (élettanász, biotechnológus) Kovács Adrienn (1989-) (molekuláris biológus) Farkas Anna (1983-) Nádró Bíborka (1992-) (általános orvos) Szentesi Péter (1967-) (élettanász) Csernoch László (1961-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
Internet cím:DOI
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4.

001-es BibID:BIBFORM056500
Első szerző:Oláh Tamás (élettanász)
Cím:Cannabinoids and muscle weakness - Investigating the function of CB1 receptors in mammalian skeletal muscle / T. Oláh, D. Bodnár, A. Tóth, J. Fodor, A. Kovács, A. Farkas, B. Nádró, P. Szentesi, L. Csernoch
Dátum:2014
Megjegyzések:The presence of CB1 cannabionid receptors (CB1R) has been shown in skeletal muscle, but it is yet to be cleared whether they have any significance in the regulation of muscle contractions. Muscle contractions are evoked by the elevation of intracellular Ca2+ concentration ([Ca2+]i) during a process called excitation-contraction coupling. CB1-mediated signaling can interefere with this process in several ways. CB1-knockout (CB1-KO) mice showed hypoactivity, however it is questionable whether this was solely originated by effects on the central nervous system or impairment of skeletal muscle function also contributes to this. It was also shown that treatment by cannabinoid agonists attenuates the contractions of frog skeletal muscle. Our aim was to study the role of CB1R in mammalian skeletal muscle, and the effects of cannabinoid drugs on Ca2+-transients.Running ability (average and maximal speed, distance) of control and CB1-KO mice was tested by activity-wheel-tests and in vivo muscle force of the animals was tested by grip-tests and hang-tests. Ca2+ transients evoked by KCl-depolarization in the presence of cannabinoid agonists were studied on enzymatically isolated flexor digitorum brevis (FDB) fibers of control and CB1-KO mice.CB1-KO mice performed worse in all the behavior tests compared to control. Depolarization-evoked Ca2+-transients were significantly higher in FDB fibers isolated from CB1-KO mice (847.8?98.2 nM, n=47) compared to control (375.6?59.9 nM, n=32, p<0.01). On control FDB the second transients after the CB1 agonist WIN55,212 treatment were significantly smaller than in untreated fibers.On the basis of the [Ca2+]i measurements we can conclude that CB1R-mediated signaling contributes to the regulation of skeletal muscle contractions, but as the main cause of the worse muscle performance of CB1-KO mice the effects mediated by the absence of CB1R in the central nervous system can neither be ruled out. These results can contribute to the identification of the side effects of medically used cannabinoid drugs on skeletal muscle.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
CB1 receptor
vázizom
Ca2+ tranziens
KO egér
Megjelenés:Acta Physiologica. - 211 : Suppl (2014), p. 82-83. -
További szerzők:Bodnár Dóra (1987-) (molekuláris biológus) Tóth Adrienn (1988-) (molekuláris biológus, élettanász) Fodor János (1973-) (élettanász, biotechnológus) Kovács Adrienn (1989-) (molekuláris biológus) Farkas Anna (1983-) Nádró Bíborka (1992-) (általános orvos) Szentesi Péter (1967-) (élettanász) Csernoch László (1961-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.4. A/2-11-1-2012-0001
TÁMOP
Internet cím:Szerző által megadott URL
DOI
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