CCL

Összesen 2 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM089414
035-os BibID:(cikkazonosító)599822 (WoS)000603609400001 (Scopus)85098499921
Első szerző:Szappanos Henrietta (biológus, élettanász)
Cím:High time resolution analysis of voltage-dependent and voltage-independent calcium sparks in frog skeletal muscle fibers / Cserne Szappanos Henrietta, Vincze János, Bodnár Dóra, Dienes Beatrix, Schneider Martin F., Csernoch László, Szentesi Péter
Dátum:2020
ISSN:1664-042X
Megjegyzések:In amphibian skeletal muscle calcium (Ca2+) sparks occur both as voltage-dependent and voltage-independent ligand-activated release events. However, whether their properties and their origin show similarities are still in debate. Elevated K+, constant Cl- content solutions were used to initiate small depolarizations of the resting membrane potential to activate dihydropyridine receptors (DHPR) and caffeine to open ryanodine receptors (RYR) on intact fibers. The properties of Ca2+ sparks observed under control conditions were compared to those measured on depolarized cells and those after caffeine treatment. Calcium sparks were recorded on intact frog skeletal muscle fibers using high time resolution confocal microscopy (x-y scan: 30 Hz). Sparks were elicited by 1 mmol/l caffeine or subthreshold depolarization to different membrane potentials. Both treatments increased the frequency of sparks and altered their morphology. Images were analyzed by custom-made computer programs. Both the amplitude (in ?F/F0; 0.259?0.001 vs. 0.164?0.001; n = 24942 and 43326, respectively; mean?SE, p<0.001) and the full width at half maximum (FWHM, in ?m; parallel with fiber axis: 2.34?0.01 vs. 1.92?0.01, p<0.001; perpendicular to fiber axis: 2.08?0.01 vs. 1.68?0.01, p<0.001) of sparks was significantly greater after caffeine treatment than on depolarized cells. 9.8% of the sparks detected on depolarized fibers and about one third of the caffeine activated sparks (29.7%) overlapped with another one on the previous frame on x-y scans. Centre of overlapping sparks travelled significantly longer distances between consecutive frames after caffeine treatment then after depolarization (in ?m; 1.66?0.01 vs. 0.95?0.01, p<0.001). Our results suggest that the two types of ryanodine receptors, the junctional RyRs controlled by DHPRs and the parajunctional RyRs are activated independently, using alternate ways, with the possibility of cooperation between neighboring release channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
skeletal muscle
Frog
excitation-contraction coupling
ryanodine Receptor
calcium-induced calcium release
Membrane depolarization
calcium spark
Caffeine
Megjelenés:Frontiers in Physiology. - 11 (2020), p. 599822. -
További szerzők:Vincze János (1947-) (biofizikus) Bodnár Dóra (1987-) (molekuláris biológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Schneider, Martin F. Csernoch László (1961-) (élettanász) Szentesi Péter (1967-) (élettanász)
Pályázati támogatás:EFOP-3.6.2- 450 16-2017-0006
EFOP
GINOP-2.3.2-15-2016-00044
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM090185
035-os BibID:(cikkazonosító)601090 (WoS)000604306200001 (Scopus)85098756322
Első szerző:Sztretye Mónika (élettanász, elektrofiziológus)
Cím:The Role of Orai1 in Regulating Sarcoplasmic Calcium Release, Mitochondrial Morphology and Function in Myostatin Deficient Skeletal Muscle / Mónika Sztretye, Zoltán Singlár, Norbert Balogh, Gréta Kis, Péter Szentesi, Ágnes Angyal, Ildikó Balatoni, László Csernoch, Beatrix Dienes
Dátum:2020
ISSN:1664-042X
Megjegyzések:In mice a naturally occurring 12-bp deletion in the myostatin gene is considered responsible for the compact phenotype (MstnCmpt?dl1Abc, Cmpt) labeled by a tremendous increase in body weight along with signs of muscle weakness, easier fatigability, decreased Orai1 expression and store operated calcium entry (SOCE). Here, on the one hand, Cmpt fibers were reconstructed with venus-Orai1 but this failed to restore SOCE. On the other hand, the endogenous Orai1 was silenced in fibers from wild type C57Bl6 mice which resulted in ?70% of Orai1 being silenced in whole muscle homogenates as confirmed by Western blot, accompanied by an inhibitory effect on the voltage dependence of SR calcium release that manifested in a slight shift toward more positive potential values. This maneuver completely hampered SOCE. Our observations are consistent with the idea that Orai1 channels are present in distinct pools responsible for either a rapid refilling of the SR terminal cisternae connected to each voltage-activated calcium transient, or a slow SOCE associated with an overall depletion of calcium in the SR lumen. Furthermore, when Cmpt cells were loaded with the mitochondrial membrane potential sensitive dye TMRE, fiber segments with depolarized mitochondria were identified covering on average 26.5 ? 1.5% of the fiber area. These defective areas were located around the neuromuscular junction and displayed significantly smaller calcium transients. The ultrastructural analysis of the Cmpt fibers revealed changes in the mitochondrial morphology. In addition, the mitochondrial calcium uptake during repetitive stimulation was higher in the Cmpt fibers. Our results favor the idea that reduced function and/or expression of SOCE partners (in this study Orai1) and mitochondrial defects could play an important role in muscle weakness and degeneration associated with certain pathologies, perhaps including loss of function of the neuromuscular junction and aging.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
SOCE
myostatin deficiency
excitation contraction coupling
mithochondrial defect
mitochondrial calcium uptake
Megjelenés:Frontiers in Physiology. - 11 (2020), p. 1-15. -
További szerzők:Singlár Zoltán (1994-) (biotechnológus) Balogh Norbert (1988-) (molekuláris biológus) Kis Gréta (1979-) (molekuláris biológus) Szentesi Péter (1967-) (élettanász) Angyal Ágnes (1987-) (molekuláris biológus) Balatoni Ildikó (1970-) (orvos) Csernoch László (1961-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus)
Pályázati támogatás:PD-108476
Egyéb
PD-128370
Egyéb
GINOP-2.3.2-15-2016-00044
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1