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001-es BibID:	BIBFORM105186
035-os BibID:	(cikkazonosító)1037230 (Scopus)85142638283 (WOS)000890212100001 (PubMed)36439266
Első szerző:	Szabó László (molekuláris biológus)
Cím:	The mechanosensitive Piezo1 channels contribute to the arterial medial calcification / Szabó, László; Balogh, Norbert; Tóth, Andrea; Angyal, Ágnes; Gönczi, Mónika; Csiki, Dávid Máté; Tóth, Csaba; Balatoni, Ildikó; Jeney, Viktória; Csernoch, László; Dienes, Beatrix
Dátum:	2022
ISSN:	1664-042X
Megjegyzések:	Vascular calcification (VC) is associated with a number of cardiovascular diseases, as well as chronic kidney disease. The role of smooth muscle cells (SMC) has already been widely explored in VC, as has the role of intracellular Ca2+ in regulating SMC function. Increased intracellular calcium concentration ([Ca2+]i) in vascular SMC has been proposed to stimulate VC. However, the contribution of the non-selective Piezo1 mechanosensitive cation channels to the elevation of [Ca2+]i, and consequently to the process of VC has never been examined. In this work the essential contribution of Piezo1 channels to arterial medial calcification is demonstrated. The presence of Piezo1 was proved on human aortic smooth muscle samples using immunohistochemistry. Quantitative PCR and Western blot analysis confirmed the expression of the channel on the human aortic smooth muscle cell line (HAoSMC). Functional measurements were done on HAoSMC under control and calcifying condition. Calcification was induced by supplementing the growth medium with inorganic phosphate (1.5 mmol/L, pH 7.4) and calcium (CaCl2, 0.6 mmol/L) for 7 days. Measurement of [Ca2+]i using fluorescent Fura-2 dye upon stimulation of Piezo1 channels (either by hypoosmolarity, or Yoda1) demonstrated significantly higher calcium transients in calcified as compared to control HAoSMCs. The expression of mechanosensitive Piezo1 channel is augmented in calcified arterial SMCs leading to a higher calcium influx upon stimulation. Activation of the channel by Yoda1 (10 ?mol/L) enhanced calcification of HAoSMCs, while Dooku1, which antagonizes the effect of Yoda1, reduced this amplification. Application of Dooku1 alone inhibited the calcification. Knockdown of Piezo1 by siRNA suppressed the calcification evoked by Yoda1 under calcifying conditions. Our results demonstrate the pivotal role of Piezo1 channels in arterial medial calcification.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk vascular smooth muscle mechanosensation Piezo1 calcification intracellular calcium concentration Yoda1 Dooku1
Megjelenés:	Frontiers in Physiology. - 13 (2022), p. 1037230. -
További szerzők:	Balogh Norbert (1988-) (molekuláris biológus) Tóth Andrea (1992-) (molekuláris biológus) Angyal Ágnes (1987-) (molekuláris biológus) Gönczi Mónika (1974-) (élettanász) Csiki Dávid Máté (1993-) (biomérnök) Tóth Csaba (1968-) (sebész, érsebész) Balatoni Ildikó (1970-) (orvos) Jeney Viktória (1971-) (vegyész, kémia tanár) Csernoch László (1961-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus)
Pályázati támogatás:	EFOP-3.6.2-16-2017-00006 EFOP TKP2020-NKA-04 Egyéb TKP2021-EGA-18 Egyéb GINOP-2.3.3-15-2016-00020 GINOP K131535 OTKA
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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
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