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001-es BibID:BIBFORM096191
035-os BibID:(cikkazonosító)9499 (scopus)85114049778 (wos)000694373200001
Első szerző:Dienes Csaba (gyógyszerész)
Cím:Electrophysiological Effects of the Transient Receptor Potential Melastatin 4 Channel Inhibitor (4-Chloro-2-(2-chlorophenoxy)acetamido) Benzoic Acid (CBA) in Canine Left Ventricular Cardiomyocytes / Csaba Dienes, Tamás Hézső, Dénes Zsolt Kiss, Dóra Baranyai, Zsigmond Máté Kovács, László Szabó, János Magyar, Tamás Bányász, Péter P. Nánási, Balázs Horváth, Mónika Gönczi, Norbert Szentandrássy
Dátum:2021
ISSN:1661-6596 1422-0067
Megjegyzések:Transient receptor potential melastatin 4 (TRPM4) plays an important role in many tissues, including pacemaker and conductive tissues of the heart, but much less is known about its electrophysiological role in ventricular myocytes. Our earlier results showed the lack of selectivity of 9-phenanthrol, so CBA ((4-chloro-2-(2-chlorophenoxy)acetamido) benzoic acid) was chosen as a new, potentially selective inhibitor. Goal: Our aim was to elucidate the effect and selectivity of CBA in canine left ventricular cardiomyocytes and to study the expression of TRPM4 in the canine heart. Experiments were carried out in enzymatically isolated canine left ventricular cardiomyocytes. Ionic currents were recorded with an action potential (AP) voltage-clamp technique in whole-cell configuration at 37 ?C. An amount of 10 mM BAPTA was used in the pipette solution to exclude the potential activation of TRPM4 channels. AP was recorded with conventional sharp microelectrodes. CBA was used in 10 ?M concentrations. Expression of TRPM4 protein in the heart was studied by Western blot. TRPM4 protein was expressed in the wall of all four chambers of the canine heart as well as in samples prepared from isolated left ventricular cells. CBA induced an approximately 9% reduction in AP duration measured at 75 and 90% of repolarization and decreased the short-term variability of APD90. Moreover, AP amplitude was increased and the maximal rates of phase 0 and 1 were reduced by the drug. In AP clamp measurements, CBA-sensitive current contained a short, early outward and mainly a long, inward current. Transient outward potassium current (Ito) and late sodium current (INa,L) were reduced by approximately 20 and 47%, respectively, in the presence of CBA, while L-type calcium and inward rectifier potassium currents were not affected. These effects of CBA were largely reversible upon washout. Based on our results, the CBA induced reduction of phase-1 slope and the slight increase of AP amplitude could have been due to the inhibition of Ito. The tendency for AP shortening can be explained by the inhibition of inward currents seen in AP-clamp recordings during the plateau phase. This inward current reduced by CBA is possibly INa,L, therefore, CBA is not entirely selective for TRPM4 channels. As a consequence, similarly to 9-phenanthrol, it cannot be used to test the contribution of TRPM4 channels to cardiac electrophysiology in ventricular cells, or at least caution must be applied.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
CBA
TRPM4
cardiac ionic currents
cardiac action potentials
canine myocytes
action potential voltage clamp
Megjelenés:International Journal Of Molecular Sciences. - 22 : 17 (2021), p. 9499. -
További szerzők:Hézső Tamás (1993-) (élettanász) Kiss Dénes Zsolt (1995-) (orvos, élettanász) Baranyai Dóra Kovács Zsigmond Máté (1995-) (orvos) Szabó László (1994-) (molekuláris biológus) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Horváth Balázs (1981-) (élettanász) Gönczi Mónika (1974-) (élettanász) Szentandrássy Norbert (1976-) (élettanász)
Pályázati támogatás:NKFIH-K115397
Egyéb
NKFIH-K138090
Egyéb
NKFIH-FK128116
Egyéb
GINOP-2.3.2-15-2016-00040
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
DE-SPACE(TKP-2020-NKA-04)
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
ÚNKP-20-3
Egyéb
ÚNKP-20-2
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM099802
035-os BibID:(cikkazonosító)917 (scopus)85122782091 (wos)000757677800001
Első szerző:Gönczi Mónika (élettanász)
Cím:Astaxanthin Exerts Anabolic Effects via Pleiotropic Modulation of the Excitable Tissue / Gönczi Mónika, Csemer Andrea, Szabó László, Sztretye Mónika, Fodor János, Pocsai Krisztina, Szenthe Kálmán, Keller-Pintér Anikó, Köhler Zoltán Márton, Nánási Péter, Szentandrássy Norbert, Pál Balázs, Csernoch László
Dátum:2022
ISSN:1661-6596 1422-0067
Megjegyzések:Astaxanthin is a lipid-soluble carotenoid influencing lipid metabolism, body weight, and insulin sensitivity. We provide a systematic analysis of acute and chronic effects of astaxanthin on different organs. Changes by chronic astaxanthin feeding were analyzed on general metabolism, expression of regulatory proteins in the skeletal muscle, as well as changes of excitation and synaptic activity in the hypothalamic arcuate nucleus of mice. Acute responses were also tested on canine cardiac muscle and different neuronal populations of the hypothalamic arcuate nucleus in mice. Dietary astaxanthin significantly increased food intake. It also increased protein levels affecting glucose metabolism and fatty acid biosynthesis in skeletal muscle. Inhibitory inputs innervating neurons of the arcuate nucleus regulating metabolism and food intake were strengthened by both acute and chronic astaxanthin treatment. Astaxanthin moderately shortened cardiac action potentials, depressed their plateau potential, and reduced the maximal rate of depolarization. Based on its complex actions on metabolism and food intake, our data support the previous findings that astaxanthin is suitable for supplementing the diet of patients with disturbances in energy homeostasis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
astaxanthin
metabolism
food intake
gene expression
skeletal muscle
cardiac action potential
arcuate nucleus
excitability
inhibitory postsynaptic current
Megjelenés:International Journal Of Molecular Sciences. - 23 : 2 (2022), p. 917. -
További szerzők:Csemer Andrea (1994-) (molekuláris biológus) Szabó László (1994-) (molekuláris biológus) Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Fodor János (1973-) (élettanász, biotechnológus) Pocsai Krisztina (1978-) (élettanász) Szenthe Kálmán Keller-Pintér Anikó Köhler Zoltán Márton Nánási Péter Pál (1956-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Pál Balázs (1975-) (élettanász) Csernoch László (1961-) (élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00040
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
NKFI FK 134684
Egyéb
NKFIH PD-128370
Egyéb
OTKA-115397
OTKA
NKFIH K 138090
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
EFOP-3.6.2-16-2017-00006
EFOP
TKP2020-IKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
TKP-2020-NKA-04
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM106081
035-os BibID:(cikkazonosító)15653 (WoS)000901106200001 (Scopus)85144543882 (PubMed)36555292
Első szerző:Singlár Zoltán (biotechnológus)
Cím:Genetic Manipulation of CB1 Cannabinoid Receptors Reveals a Role in Maintaining Proper Skeletal Muscle Morphology and Function in Mice / Singlár Zoltán, Ganbat Nyamkhuu, Szentesi Péter, Osgonsandag Nomin, Szabó László, Telek Andrea, Fodor János, Dienes Beatrix, Gönczi Mónika, Csernoch László, Sztretye Mónika
Dátum:2022
ISSN:1422-0067
Megjegyzések:The endocannabinoid system (ECS) refers to a widespread signaling system and its alteration is implicated in a growing number of human diseases. Cannabinoid receptors (CBRs) are highly expressed in the central nervous system and many peripheral tissues. Evidence suggests that CB1Rs are expressed in human and murine skeletal muscle mainly in the cell membrane, but a subpopulation is present also in the mitochondria. However, very little is known about the latter population. To date, the connection between the function of CB1Rs and the regulation of intracellular Ca2+ signaling has not been investigated yet. Tamoxifen-inducible skeletal muscle-specific conditional CB1 knock-down (skmCB1-KD, hereafter referred to as Cre(+/-)) mice were used in this study for functional and morphological analysis. After confirming CB1R down-regulation on the mRNA and protein level, we performed in vitro muscle force measurements and found that peak twitch, tetanus, and fatigue were decreased significantly in Cre(+/-) mice. Resting intracellular calcium concentration, voltage dependence of the calcium transients as well as the activity dependent mitochondrial calcium uptake were essentially unaltered by Cnr1 gene manipulation. Nevertheless, we found striking differences in the ultrastructural architecture of the mitochondrial network of muscle tissue from the Cre(+/-) mice. Our results suggest a role of CB1Rs in maintaining physiological muscle function and morphology. Targeting ECS could be a potential tool in certain diseases, including muscular dystrophies where increased endocannabinoid levels have already been described.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
endocannabinoid system (ECS)
cannabinoid receptor of type 1 (CBR1)
skeletal muscle force
contractility
excitation-contraction coupling (ECC)
mitochondria
intracellular calcium
Megjelenés:International Journal Of Molecular Sciences. - 23 : 24 (2022), p. 1-21. -
További szerzők:Ganbat, Nyamkhuu Szentesi Péter (1967-) (élettanász) Osgonsandag, Nomin Szabó László (1994-) (molekuláris biológus) Telek Andrea (1977-) (élettanász) Fodor János (1973-) (élettanász, biotechnológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Gönczi Mónika (1974-) (élettanász) Csernoch László (1961-) (élettanász) Sztretye Mónika (1981-) (élettanász, elektrofiziológus)
Pályázati támogatás:NKFIH-FK-142481
Egyéb
NKFIH K-137600
Egyéb
NKFIH 2019-2.1.11-TÉT-2019-00063
Egyéb
ÚNKP-22-3-II-DE-239
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
TKP2021-EGA-18
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM114566
035-os BibID:(cikkazonosító)13536 (scopus)85170341617 (wos)001061092600001
Első szerző:Szabó László (molekuláris biológus)
Cím:Reduced Expression of Septin7 Hinders Skeletal Muscle Regeneration / Szabó László, Telek Andrea, Fodor János, Dobrosi Nóra, Dócs Klaudia, Hegyi Zoltán, Gönczi Mónika, Csernoch László, Dienes Beatrix
Dátum:2023
ISSN:1422-0067
Megjegyzések:Septins are considered the fourth component of the cytoskeleton with the septin7 isoform playing a critical role in the formation of diffusion barriers in phospholipid bilayers and intra- and extracellular scaffolds. While its importance has already been confirmed in different intracellular processes, very little is known about its role in skeletal muscle. Muscle regeneration was studied in a Sept7 conditional knock-down mouse model to prove the possible role of septin7 in this process. Sterile inflammation in skeletal muscle was induced which was followed by regeneration resulting in the upregulation of septin7 expression. Partial knock-down of Sept7 resulted in an increased number of inflammatory cells and myofibers containing central nuclei. Taken together, our data suggest that partial knock-down of Sept7 hinders the kinetics of muscle regeneration, indicating its crucial role in skeletal muscle functions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
septin7
skeletal muscle
regeneration
central nuclei
muscle injury
Megjelenés:International Journal Of Molecular Sciences. - 24 : 17 (2023), p. 13536. -
További szerzők:Telek Andrea (1977-) (élettanász) Fodor János (1973-) (élettanász, biotechnológus) Dobrosi Nóra (1981-) (molekuláris biológus) Dócs Klaudia (1989-) (orvos) Hegyi Zoltán (1983-) (molekuláris biológus) Gönczi Mónika (1974-) (élettanász) Csernoch László (1961-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus)
Pályázati támogatás:NKFIH K-137600
Egyéb
TKP2020-NKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
TKP2021-EGA-18
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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