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001-es BibID:	BIBFORM009063
Első szerző:	Alvarez, Julio
Cím:	ATP/UTP activate cation-permeable channels with TRPC3/7 properties in rat cardiomyocytes / Alvarez, J., Coulombe, A., Cazorla, O., Ugur, M., Rauzier, J. M., Magyar, J., Mathieu, E. L., Boulay, G., Souto, R., Bideaux, P., Salazar, G., Rassendren, F., Lacampagne, A., Fauconnier, J., Vassort, G.
Dátum:	2008
ISSN:	0363-6135 (Print)
Megjegyzések:	Extracellular purines and pyrimidines have major effects on cardiac rhythm and contraction. ATP/UTP are released during various physiopathological conditions, such as ischemia, and despite degradation by ectonucleotidases, their interstitial concentrations can markedly increase, a fact that is clearly associated with arrhythmia. In the present whole cell patch-clamp analysis on ventricular cardiomyocytes isolated from various mammalian species, ATP and UTP elicited a sustained, nonselective cationic current, I(ATP). UDP was ineffective, whereas 2'(3')-O-(4-benzoylbenzoyl)-ATP was active, suggesting that P2Y(2) receptors are involved. I(ATP) resulted from the binding of ATP(4-) to P2Y(2) purinoceptors. I(ATP) was maintained after ATP removal in the presence of guanosine 5'-[gamma-thio]triphosphate and was inhibited by U-73122, a PLC inhibitor. Single-channel openings are rather infrequent under basal conditions. ATP markedly increased opening probability, an effect prevented by U-73122. Two main conductance levels of 14 and 23 pS were easily distinguished. Similarly, in fura-2-loaded cardiomyocytes, Mn(2+) quenching and Ba(2+) influx were significant only in the presence of ATP or UTP. Adult rat ventricular cardiomyocytes expressed transient receptor potential channel TRPC1, -3, -4, and -7 mRNA and the TRPC3 and TRPC7 proteins that coimmunoprecipitated. Finally, the anti-TRPC3 antibody added to the patch pipette solution inhibited I(ATP). In conclusion, activation of P2Y(2) receptors, via a G protein and stimulation of PLCbeta, induces the opening of heteromeric TRPC3/7 channels, leading to a sustained, nonspecific cationic current. Such a depolarizing current could induce cell automaticity and trigger the arrhythmic events during an early infarct when ATP/UTP release occurs. These results emphasize a new, potentially deleterious role of TRPC channel activation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Adenosine Triphosphate Animals Arrhythmias, Cardiac Cell Membrane Permeability Disease Models, Animal Dogs Estrenes Humans Male Membrane Potentials Mice Mice, Knockout Myocardial Infarction Myocytes, Cardiac Patch-Clamp Techniques Phosphodiesterase Inhibitors Phospholipase C beta Pyrrolidinones Rats Rats, Wistar Receptors, Purinergic P2 Signal Transduction TRPC Cation Channels Uridine Triphosphate
Megjelenés:	American Journal of Physiology. Heart and Circulatory Physiology. - 295 (2008), p. H21-H28. -
További szerzők:	Coulombe, Alaine Cazorla, Olivier Ugur, Mehmet Rauzier, Jean-Michel Magyar János (1961-) (élettanász) Mathieu, Eve-Lyne Boulay, Guylain Souto, Rafael Bideaux, Patrice Salazar, Guillermo Rassendren, Francois Lacampagne, Alain Fauconnier, Jérémy Vassort, Guy
Internet cím:	DOI elektronikus változat
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001-es BibID:	BIBFORM032937
035-os BibID:	PMID:17158651
Első szerző:	Schroder, Elizabeth
Cím:	Chronic verapamil treatment remodels ICa,L in mouse ventricle / Elizabeth Schroder, Janos Magyar, Don Burgess, Douglas Andres, Jonathan Satin
Dátum:	2007
ISSN:	0363-6135
Megjegyzések:	In this study we tested the hypothesis that ventricular homeostasis of L-type Ca(2+) current (I(Ca,L)) minimally involves regulation of the main pore-forming alpha-subunit (Ca(V)1.2) and auxiliary proteins that serve as positive or negative regulators of I(Ca,L). We treated animals for 24 h with verapamil (Ver, 3.6 mg.kg(-1).day(-1)), isoproterenol (Iso, 30 mg.kg(-1).day(-1)), or Iso + Ver via osmotic minipumps. To test for alterations of Ca(2+) channel complex components we performed real-time PCR and Western blot analysis on ventricle. In addition, cardiac myocytes (CMs) were dispersed and current was recorded in the whole cell configuration to evaluate I(Ca,L). Surprisingly, 24- to 48-h Ver increased Ca(V)1.2 mRNA and protein and I(Ca,L) current (Ver 11 +/- 1pA/pF vs. control 7 +/- 0.5pA/pF; P < 0.01). I(Ca,L) from CMs in Ver mice showed no change in whole cell capacitance. To examine the in vivo effects of a physiologically relevant Ca(2+) channel agonist, we treated mice with Iso. Twenty-four-hour Iso infusion increased heart rate; Ca(V)1.2- and Ca(V)beta(2) mRNA levels were constant, but the Ca(2+) channel subunit mRNA Rem was increased twofold. Cells isolated from 24-h Iso hearts showed no change in basal I(Ca,L) density and diminished responsiveness to acute 1 muM Iso. To further examine the homeostatic regulation of the Ca(2+) channel, we treated animals for 24 h with Iso + Ver. The influence of Iso + Ver was similar that of to Iso alone on Ca(2+) channel mRNAs and I(Ca,L), with the exception that it prevented the increase in Rem seen with Iso treatment. Long-term Ca(2+) channel blockade induces an increase of Ca(V)1.2 mRNA and protein and significantly increases I(Ca,L).
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	American Journal of Physiology-Heart And Circulatory Physiology 292 : 4 (2007), p. H1906-H1916. -
További szerzők:	Magyar János (1961-) (élettanász) Burgess, Don E. Andres, Douglas Satin, Jonathan
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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