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001-es BibID:BIBFORM057406
Első szerző:Magyar János (élettanász)
Cím:Role of Gap Junction Channel in the Development of Beat-to-Beat Action Potential Repolarization Variability and Arrhythmias / János Magyar, Tamás Bányász, Norbert Szentandrássy, Kornél Kistamás, Péter P. Nánási, Jonathan Satin
Dátum:2015
ISSN:1381-6128
Megjegyzések:The short-term beat-to-beat variability of cardiac action potential duration (SBVR) occurs as a random alteration of the ventricular repolarization duration. SBVR has been suggested to be more predictive of the development of lethal arrhythmias than the action potential prolongation or QT prolongation of ECG alone. The mechanism underlying SBVR is not completely understood but it is known that SBVR depends on stochastic ion channel gating, intracellular calcium handling and intercellular coupling. Coupling of single cardiomyocytes significantly decreases the beat-to-beat changes in action potential duration (APD) due to the electrotonic current flow between neighboring cells. The magnitude of this electrotonic current depends on the intercellular gap junction resistance. Reduced gap junction resistance causes greater electrotonic current flow between cells, and reduces SBVR. Myocardial ischaemia (MI) is known to affect gap junction channel protein expression and function. MI increases gap junction resistance that leads to slow conduction, APD and refractory period dispersion, and an increase in SBVR. Ultimately, development of reentry arrhythmias and fibrillation are associated post-MI. Antiarrhythmic drugs have proarrhythmic side effects requiring alternative approaches. A novel idea is to target gap junction channels. Specifically, the use of gap junction channel enhancers and inhibitors may help to reveal the precise role of gap junctions in the development of arrhythmias. Since cell-to-cell coupling is represented in SBVR, this parameter can be used to monitor the degree of coupling of myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Heart
gap junction
beat-to-beat variability
arrhythmia
Megjelenés:Current Pharmaceutical Design. - 21 : 8 (2015), p. 1042-1052. -
További szerzők:Bányász Tamás (1960-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Kistamás Kornél (1986-) (biológus) Nánási Péter Pál (1956-) (élettanász) Satin, Jonathan
Pályázati támogatás:K109736
OTKA
K100151
OTKA
PD101171
OTKA
K101196
OTKA
NK104331
OTKA
TÁMOP-4.2.4.A/2-11/1-2012-0001
TÁMOP
Internet cím:Szerző által megadott URL
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2.

001-es BibID:BIBFORM032928
035-os BibID:WOS:000225354300015
Első szerző:Magyar János (élettanász)
Cím:Divergent action potential morphologies reveal nonequilibrium properties of human cardiac Na channels / János Magyar, Carmen E. Kiper, Robert Dumaine, Don E. Burgess, Tamás Bányász, Jonathan Satin
Dátum:2004
ISSN:0008-6363
Megjegyzések:Objective: Fast inward Na current (INa) carried by the voltage-gated Na channel (NaV1.5) is critical for action potential (AP) propagation and the rapid upstroke of the cardiac AP. In addition, a small fraction of NaV1.5 channels remains open throughout the plateau of the AP, and this current is termed as late INa. In patients with mutant NaV1.5-based congenital long Q?T (LQT) syndrome, mutant channels pass more late INa compared to wild-type channels in unaffected patients. Although LQT mutant NaV1.5 channels are well studied, there is no careful evaluation of the effects of cardiac APs on early and late current. This is important with the recent documentation of nonequilibrium INa.Methods: We measured AP-stimulated INa through NaV1.5 wild-type and two LQT mutant channels (?KPQ and N1325S). Three distinct AP morphologies were used: human embryonic stem cell-derived cardiac myocyte (hES-CM) APs with a relatively slow upstroke and canine endocardial and epicardial ventricular myocytes with rapid upstrokes.Results: All three APs elicited both early and late INa. For wild-type NaV1.5, the hES-CM AP elicits more early and late INa than either the endocardial or epicardial AP. The mechanism for this difference is that the hES-CM has a relative slow dV/dtmax that causes a maximal open channel probability. Slower upstroke stimulation also allows greater Na flux through wild-type and N1325S channels, but not the ?KPQ mutant.Conclusions: The inherent gating properties of NaV1.5 provide natural tuning of optimal INa density. Slower upstroke velocities can yield more INa and Na flux in some NaV1.5 variants.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cardiovascular Research. - 64 : 3 (2004), p. 477-487. -
További szerzők:Kiper, Carmen E. Dumaine, Robert Burgess, Don E. Bányász Tamás (1960-) (élettanász) Satin, Jonathan
Pályázati támogatás:OTKA-T043182
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM020232
035-os BibID:(Scopus)80051997255 (WoS)000294414700010
Első szerző:Magyar János (élettanász)
Cím:Long term regulation of cardiac L-type calcium channel by small G proteins / Magyar J., Jenes A., Kistamas K., Ruzsnavszky F., Nanasi P. P., Satin J., Szentandrassy N., Banyasz T.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Calcium ions are crucial elements of excitation-contraction coupling in cardiac myocytes. The intracellular Ca(2+) concentration changes continously during the cardiac cycle, but the Ca(2+) entering to the cell serves as an intracellular second messenger, as well. The Ca(2+) as a second messenger influences the activity of many intracellular signalling pathways and regulates gene expression. In cardiac myocytes the major pathway for Ca(2+) entry into cells is L-type calcium channel (LTCC). The precise control of LTCC function is essential for maintaining the calcium homeostasis of cardiac myocytes. Dysregulation of LTCC may result in different diseases like cardiac hypertrophy, arrhytmias, heart failure. The physiological and pathological structural changes in the heart are induced in part by small G proteins. These proteins are involved in wide spectrum of cell biological functions including protein transport, regulation of cell proliferation, migration, apoptosis, and cytoskeletal rearrangement. Understanding the crosstalk between small G proteins and LTCC may help to understand the pathomechanism of different cardiac diseases and to develop a new generation of genetically-encoded Ca(2+) channel inhibitors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3714-3719. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Kistamás Kornél (1986-) (biológus) Ruzsnavszky Ferenc (1984-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Satin, Jonathan Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
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