CCL

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

1.

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:

2.

001-es BibID:BIBFORM083077
035-os BibID:(cikkazonosító)98 (WOS)000519877100052 (Scopus)85078738942 (PMID)31979219
Első szerző:Sztretye Mónika (élettanász, elektrofiziológus)
Cím:Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle / Mónika Sztretye, Zoltán Singlár, László Szabó, Ágnes Angyal, Norbert Balogh, Faranak Vakilzadeh, Péter Szentesi, Beatrix Dienes, László Csernoch
Dátum:2020
ISSN:2076-3921
Megjegyzések:BACKGROUND: Astaxanthin (AX) a marine carotenoid is a powerful natural antioxidant which protects against oxidative stress and improves muscle performance. Retinol and its derivatives were described to affect lipid and energy metabolism. Up to date, the effects of AX and retinol on excitation-contraction coupling (ECC) in skeletal muscle are poorly described. METHODS: 18 C57Bl6 mice were divided into two groups: Control and AX supplemented in rodent chow for 4 weeks (AstaReal A1010). In vivo and in vitro force and intracellular calcium homeostasis was studied. In some experiments acute treatment with retinol was employed. RESULTS: The voltage activation of calcium transients (V50) were investigated in single flexor digitorum brevis isolated fibers under patch clamp and no significant changes were found following AX supplementation. Retinol shifted V50 towards more positive values and decreased the peak F/F0 of the calcium transients. The amplitude of tetani in the extensor digitorum longus was significantly higher in AX than in control group. Lastly, the mitochondrial calcium uptake was found to be less prominent in AX. CONCLUSION: AX supplementation increases in vitro tetanic force without affecting ECC and exerts a protecting effect on the mitochondria. Retinol treatment has an inhibitory effect on ECC in skeletal muscle.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
skeletal muscle
intracellular calcium
mitochondrial calcium
excitation contraction coupling
force
astaxanthin
retinol
Megjelenés:Antioxidants. - 9 : 2 (2020), p. 98. -
További szerzők:Singlár Zoltán (1994-) (biotechnológus) Szabó László (1994-) (molekuláris biológus) Angyal Ágnes (1987-) (molekuláris biológus) Balogh Norbert (1988-) (molekuláris biológus) Vakilzadeh, Faranak Szentesi Péter (1967-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Csernoch László (1961-) (élettanász)
Pályázati támogatás:NKFIH-1150-6/2019
Egyéb
NKFIH PD-128370
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:
Rekordok letöltése1