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1.

001-es BibID:BIBFORM010417
Első szerző:Borbély Attila (kardiológus)
Cím:Transcriptional and posttranslational modifications of titin : implications for diastole / Borbely, A., van Heerebeek, L., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztőségi anyag
Alternative Splicing
Animals
Cyclic AMP-Dependent Protein Kinases
Cyclic GMP-Dependent Protein Kinases
Diabetes Complications
Diacetyl
derivatives
Diastole
Elasticity
Extracellular Matrix
Gelsolin
Heart Failure, Diastolic
Humans
Mice
Muscle Proteins
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Protein Processing, Post-Translational
Rats
Sarcomeres
Triiodothyronine
Ventricular Remodeling
Megjelenés:Circulation Research. - 104 : 1 (2009), p. 12-14. -
További szerzők:Heerebeek, Loek, van Paulus, Walter J.
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DOI
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2.

001-es BibID:BIBFORM010415
Első szerző:Borbély Attila (kardiológus)
Cím:Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium / Borbely, A., Falcao-Pires, I., van Heerebeek, L., Hamdani, N., Edes, I., Gavina, C., Leite-Moreira, A. F., Bronzwaer, J. G. F., Papp, Z., van der Velden, J., Stienen, G. J. M., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Megjegyzések:High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of isolated cardiomyocytes to expression of titin isoforms and to phosphorylation of titin and titin isoforms. Biopsies were procured by transvascular technique (44 HF, 3 CON), perioperatively (25 AS, 4 CON), or from explanted hearts (4 HF, 8 CON). None had coronary artery disease. Isolated, permeabilized cardiomyocytes were stretched to 2.2-microm sarcomere length to measure F(passive). Expression and phosphorylation of titin isoforms were analyzed using gel electrophoresis with ProQ Diamond and SYPRO Ruby stains and reported as ratio of titin (N2BA/N2B) or of phosphorylated titin (P-N2BA/P-N2B) isoforms. F(passive) was higher in HF (6.1+/-0.4 kN/m(2)) than in CON (2.3+/-0.3 kN/m(2); P<0.01) or in AS (2.2+/-0.2 kN/m(2); P<0.001). Titin isoform expression differed between HF (N2BA/N2B=0.73+/-0.06) and CON (N2BA/N2B=0.39+/-0.05; P<0.001) and was comparable in HF and AS (N2BA/N2B=0.59+/-0.06). Overall titin phosphorylation was also comparable in HF and AS, but relative phosphorylation of the stiff N2B titin isoform was significantly lower in HF (P-N2BA/P-N2B=0.77+/-0.05) than in AS (P-N2BA/P-N2B=0.54+/-0.05; P<0.01). Relative hypophosphorylation of the stiff N2B titin isoform is a novel mechanism responsible for raised F(passive) of human HF cardiomyocytes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Aged
Biopsy
Elasticity
Female
Heart Failure
Humans
Male
Middle Aged
Muscle Proteins
Myocardium
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Sarcomeres
Megjelenés:Circulation Research. - 104 : 6 (2009), p. 780-786. -
További szerzők:Falcao-Pires, Ines Heerebeek, Loek, van Hamdani, Nazha Édes István (1952-) (kardiológus) Gavina, Cristina Leite-Moreira, Adelino F. Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Velden, Jolanda, van der Stienen, Ger J. M. Paulus, Walter J.
Internet cím:DOI
elektronikus változat
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3.

001-es BibID:BIBFORM023031
Első szerző:Jeney Viktória (vegyész, kémia tanár)
Cím:Role of Antioxidant-1 in Extracellular Superoxide Dismutase Function and Expression / Viktoria Jeney, Shinichi Itoh, Maria Wendt, Quinton Gradek, Masuko Ushio-Fukai, David G. Harrison, Tohru Fukai
Dátum:2005
ISSN:0009-7330
Megjegyzések:The extracellular superoxide dismutase (ecSOD or SOD3) is a copper-containing enzyme which is highly expressed in the vasculature. Copper-containing enzymes require copper chaperones for their activity however the chaperone which delivers copper to SOD3 has not previously been defined. Atox1 is a copper chaperone proposed to deliver copper to the trans-Golgi network. Because SOD3 is secreted via the trans-Golgi network, we sought to determine whether Atox1 acts as a copper chaperone for SOD3. Using recombinant human SOD3, we found that the specific activity of SOD3 directly correlates with its copper content (R-2 = 0.99). SOD3 specific activity in the conditioned medium from cultured Atox1(-/-) fibroblasts was markedly decreased, but could be recovered to that of wild-type cells by copper addition. These results indicated that Atox1 is required for delivering copper to SOD3 for its full activity. Unexpectedly, the protein and mRNA levels of SOD3 were dramatically decreased in cultured Atox1(-/-) fibroblasts. This was associated with a marked decrease in SOD3 transcription rate but no change in SOD3 mRNA stability. Overexpression of Atox1 markedly increased SOD3 mRNA in both Atox1(-/-) and Atox1(-/-) cells. These findings indicate that Atox1 positively regulates SOD3 transcription. Because SOD3 protein is upregulated in atherosclerotic vessels, we examined expression of Atox1 in vessels from ApoE(-/-) mice. Western and immunohistochemical analysis in ApoE(-/-) mice revealed that both Atox1 and SOD3 protein levels are markedly increased in atherosclerotic intimal lesions. In summary, Atox1 functions not only as a copper chaperone for SOD3 but also as a positive regulator for SOD3 transcription and may have an important role in modulating oxidative stress in the cardiovascular system.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 96 : 7 (2005), p. 723-729. -
További szerzők:Itoh, Shinichi Wendt, Maria Gradek, Quinton Ushio-Fukai, Masuko Harrison, David G. Fukai, Tohru
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4.

001-es BibID:BIBFORM090647
Első szerző:Kiss Éva
Cím:Thyroid Hormone-Induced Alterations in Phospholamban-Deficient Mouse Hearts / Kiss Eva, Brittsan Angie G., Edes Istvan, Grupp Ingrid L., Grupp Gunter, Kranias Evangelia G.
Dátum:1998
ISSN:0009-7330
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Circulation Research. - 83 : 6 (1998), p. 608-613. -
További szerzők:Brittsan, Angie G. Édes István (1952-) (kardiológus) Grupp, Ingrid L. Grupp, Gunter Kranias, Evangelia G.
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5.

001-es BibID:BIBFORM023034
Első szerző:Nguyen, Andrew D.
Cím:Fibulin-5 Is a Novel Binding Protein for Extracellular Superoxide Dismutase / Andrew D. Nguyen, Shinichi Itoh, Viktoria Jeney, Hiromi Yanagisawa, Mitsuaki Fujimoto, Masuko Ushio-Fukai, Tohru Fukai
Dátum:2004
ISSN:0009-7330
Megjegyzések:The extracellular superoxide dismutase (ecSOD) plays an important role in atherosclerosis and endothelial function by modulating levels of the superoxide anion (O-2(.-)) in the extracellular space. Although heparan sulfate proteoglycan is an important ligand for ecSOD, little is known about other biological binding partners of ecSOD. The goal of this study was to identify novel proteins that interact with ecSOD. A yeast two-hybrid screening of a human aorta cDNA library using ecSOD as bait identified fibulin-5 as a predominant binding protein for ecSOD. Further analysis showed that the binding domain of ecSOD within fibulin-5 mapped to its C-terminal domain. In vitro pulldown assays and coimmunoprecipitation analysis further confirmed that ecSOD interacts with fibulin-5 in vitro and in vivo. Studies using fibulin-5(-/-) mice indicated that fibulin-5 is required for binding of ecSOD to vascular tissue. Importantly, the decrease in tissue-bound ecSOD levels in aortas from fibulin-5(-/-) mice was associated with an increase in vascular O-2(.-) levels. Furthermore, immunohistochemical analysis using ApoE(-/-) mice suggested a codistribution of ecSOD and fibulin-5 in atherosclerotic vessels. In summary, we provide in this study the first evidence that the ecSOD-fibulin-5 interaction is required for ecSOD binding to vascular tissues, thereby regulating vascular O-2(.-) levels. This interaction may represent a novel mechanism for controlling vascular redox state in the extracellular space in various cardiovascular diseases such as atherosclerosis and hypertension in which oxidative stress is increased.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 95 : 11 (2004), p. 1067-1074. -
További szerzők:Itoh, Shinichi Jeney Viktória (1971-) (vegyész, kémia tanár) Yanagisawa, Hiromi Fujimoto, Mitsuaki Ushio-Fukai, Masuko Fukai, Tohru
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6.

001-es BibID:BIBFORM101157
035-os BibID:(WOS)000639308800011 (Scopus)85103228803 (PubMed)33601939
Első szerző:Shimkunas, Rafael
Cím:Mechanical Load Regulates Excitation-Ca2+ Signaling-Contraction in Cardiomyocyte / Rafael Shimkunas, Bence Hegyi , Zhong Jian, John A. Shaw, Mohammad A. Kazemi-Lari, Debika Mitra, J. Kent Leach, Xiaocen Li, Mark Jaradeh, Nicholas Balardi, Yi-Je Chen, Ariel L. Escobar, Anthony J. Baker, Julie Bossuyt, Tamas Banyasz, Nipavan Chiamvimonvat, Kit S. Lam, Donald M. Bers, Leighton T. Izu, Ye Chen-Izu
Dátum:2021
ISSN:0009-7330
Tárgyszavak:Orvostudományok Elméleti orvostudományok levél
folyóiratcikk
polythene glycol
muscle contraction
stress, mechanical
mechanotransduction, cellular
hydrogels
sarcomere
calcium signaling
myocytes, cardiac
action potentials
Megjelenés:Circulation Research. - 128 : 6 (2021), p. 772-774. -
További szerzők:Hegyi Bence (1987-) (élettanász) Jian, Zhong Shaw, John A. Kazemi-Lari, Mohammad Mitra, Debika Leach, J. Kent Li, Xiaocen Jaradeh, Mark Balardi, Nicholas Chen, Yi-Je Escobar, Ariel L. Baker, Anthony J. Bossuyt, Julie Bányász Tamás (1960-) (élettanász) Chiamvimonvat, Nipavan Lam, Kit S. Bers, Donald M. Izu, Leighton T. Chen-Izu, Ye
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7.

001-es BibID:BIBFORM046567
035-os BibID:PMID:15388639
Első szerző:Szentesi Péter (élettanász)
Cím:Sarcoplasmic reticulum Ca2+ refilling controls recovery from Ca2+-induced Ca2+ release refractoriness in heart muscle / Peter Szentesi, Christophe Pignier, Marcel Egger, Evangelia G. Kranias, Ernst Niggli
Dátum:2004
ISSN:0009-7330
Megjegyzések:In cardiac muscle Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) is initiated by Ca2+ influx via L-type Ca2+ channels. At present, the mechanisms underlying termination of SR Ca2+ release, which are required to ensure stable excitation-contraction coupling cycles, are not precisely known. However, the same mechanism leading to refractoriness of SR Ca2+ release could also be responsible for the termination of CICR. To examine the refractoriness of SR Ca2+ release, we analyzed Na+-Ca2+ exchange currents reflecting cytosolic Ca2+ signals induced by UV-laser flash-photolysis of caged Ca2+. Pairs of UV flashes were applied at various intervals to examine the time course of recovery from CICR refractoriness. In cardiomyocytes isolated from guinea-pigs and mice, beta-adrenergic stimulation with isoproterenol-accelerated recovery from refractoriness by approximately 2-fold. Application of cyclopiazonic acid at moderate concentrations (<10 micromol/L) slowed down recovery from refractoriness in a dose-dependent manner. Compared with cells from wild-type littermates, those from phospholamban knockout (PLB-KO) mice exhibited almost 5-fold accelerated recovery from refractoriness. Our results suggest that SR Ca2+ refilling mediated by the SR Ca2+-pump corresponds to the rate-limiting step for recovery from CICR refractoriness. Thus, the Ca2+ sensitivity of CICR appears to be regulated by SR Ca2+ content, possibly resulting from a change in the steady-state Ca2+ sensitivity and in the gating kinetics of the SR Ca2+ release channels (ryanodine receptors). During Ca2+ release, the concomitant reduction in Ca2+ sensitivity of the ryanodine receptors might also underlie Ca2+ spark termination by deactivation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 95 : 8 (2004), p. 807-813. -
További szerzők:Pignier, Christophe Egger, Marcel Kranias, Evangelia G. Niggli, Ernst
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8.

001-es BibID:BIBFORM018115
Első szerző:Szerafin Tamás (szívsebész, mellkassebész)
Cím:Increased cyclooxygenase-2 expression and prostaglandin-mediated dilation in coronary arterioles of patients with diabetes mellitus / Szerafin T., Erdei N., Fülöp T., Pasztor T. E., Edes I., Koller A., Bagi Z.
Dátum:2006
ISSN:0009-7330
Megjegyzések:Based on findings of experimental models of diabetes mellitus (DM) showing increased expression of vascular cyclooxygenase-2 (COX-2), we hypothesized that in patients with DM changes in COX-2-dependent prostaglandin synthesis affect vasomotor responses of coronary arterioles. Arterioles were dissected from the right atrial appendages obtained at the time of cardiac surgery of patient with DM(+) or without documented diabetes DM(-). Isolated arterioles (89+/-15 microm in diameter) were cannulated and pressurized (at 80 mm Hg), and changes in diameter were measured with video microscopy. After spontaneous tone developed [DM(-): 32+/-7%; DM(+): 37+/-5%; P=NS], arteriolar responses to bradykinin were investigated. Dilations to bradykinin (0.1 nmol/L to 1 micromol/L) were significantly (P<0.05) greater in DM(+) than DM(-) patients (10 nmol/L: 77+/-10% versus 38+/-14%). In both groups, dilations were similar to the NO-donor, sodium nitroprusside. In arterioles of DM(+), but not those of DM(-), patients' bradykinin-induced dilations were reduced by the nonselective COX inhibitor indomethacin or by the selective COX-2 inhibitor NS-398 (DM(+) at 10 nmol/L: to 20+/-4% and 29+/-7%, respectively). Correspondingly, a marked COX-2 immunostaining was detected in coronary arterioles of DM(+), but not in those of DM(-) patients. We conclude that in coronary arterioles of diabetic patients bradykinin induces enhanced COX-2-derived prostaglandin-mediated dilation. These findings are the first to show that in humans diabetes mellitus increases COX-2 expression and dilator prostaglandin synthesis in coronary arterioles, which may serve to increase dilator capacity and maintain adequate perfusion of cardiac tissues.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 99 : 5 (2006), p. e12-e17. -
További szerzők:Erdei Nóra (1979-) (orvos) Fülöp Tibor (1957-) (kardiológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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