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1.

001-es BibID:BIBFORM029128
Első szerző:Beleznai Tímea (orvos)
Cím:Activation of hexosamine pathway impairs nitric oxide (NO)-dependent arteriolar dilations by increased protein O-GlcNAcylation / Beleznai Timea, Bagi Zsolt
Dátum:2012
ISSN:1537-1891
Megjegyzések:We hypothesized that under high glucose conditions, activation of the hexosamine pathway leads to impaired nitric oxide (NO)-dependent arteriolar dilation. Skeletal muscle arterioles (diameter: ~160mikrom) isolated from male Wistar rats were exposed to normal glucose (NG, 5.5mmol/L) or high glucose concentrations (HG, 30mmol/L, for 2h) and agonist-induced diameter changes were measured with videomicroscopy. Western blots were performed to identify the vascular levels of protein O-linked-N-acetyl-glucosamine (O-GlcNAc) and phosphorylated endothelial NO synthase (eNOS). In arterioles exposed to HG, dilations to histamine were abolished compared to those exposed to NG (max: -6±6% and 69±9%, respectively), while acetylcholine-induced responses were not affected. Inhibition of NO synthesis with N(G)-nitro-l-arginine methyl ester (L-NAME) reduced histamine-induced dilations in NG arterioles, but it had no effect on microvessels exposed to HG. Dilations to the NO donor, sodium nitroprusside and constrictions to norepinephrine and serotonin were similar in the two groups. In the presence of the inhibitor of hexosamine pathway, azaserine, histamine-induced dilations were significantly augmented in arterioles exposed to HG (max: 67±2%). Moreover, exposure of vessels to glucosamine (5mmol/L, for 2h) resulted in reduced histamine-induced arteriolar dilations (max: 26±3%). The level of protein O-GlcNAcylation was increased, whereas the P-eNOS (Ser-1177) was decreased in HG exposed vessels. These findings indicate that a high concentration of glucose may lead to glucosamine formation, which impairs histamine-induced, NO-mediated arteriolar dilations. We propose that interfering with the hexosamine pathway may prevent microvascular complications in diabetes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Vascular Pharmacology. - 56 : 3-4 (2012), p. 115-121. -
További szerzők:Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:RE/08/004
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM030263
035-os BibID:WOS:000168774300010
Első szerző:Jednákovits Andrea
Cím:In vivo and in vitro acute cardiovascular effects of bimoclomol / Andrea Jednákovits, Péter Ferdinándy, László Jaszlits, Tamás Bányász, János Magyar, Péter Szigligeti, Ágnes Körtvély, József A. Szentmiklósi, Péter P. Nánási
Dátum:2000
ISSN:0306-3623
Megjegyzések:Effects of bimoclomol, the novel heat shock protein (HSP) coinducer, was studied in various mammalian cardiac and rabbit aortic preparations. Bimoclomol decreased the ST-segment elevation induced by coronary occlusion in anesthetized dogs (56% and 80% reduction with 1 and 5 mg/kg, respectively). In isolated working rat hearts, bimoclomol increased coronary now (CF), decreased the reduction of cardiac output (CO) and left ventricular developed pressure (LVDP) developing after coronary occlusion, and prevented ventricular fibrillation (VF) during reperfusion. In rabbit aortic preparations, precontracted with phenylephrine, bimoclomol induced relaxation (EC50=214 muM). Bimoclomol produced partial relaxation against 20 mM KCl, however, bimoclomol failed to relax preparations precontracted with serotonin, PGF(2) or angiotensin II. All these effects were evident within a few minutes after application of bimoclomol. A rapid bimoclomol-induced compartmental translocation of the already preformed HSPs may explain the protective action of the compound. (C) 2001 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Pharmacology-the Vascular System. - 34 : 5 (2000), p. 363-369. -
További szerzők:Ferdinándy Péter Jaszlits László Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigligeti Péter Körtvély Ágnes Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM030336
035-os BibID:PMID: 15320833
Első szerző:Mohácsi Attila (orvos)
Cím:Effects of endothelins on cardiac and vascular cells : new therapeutic target for the future? / Attila Mohácsi, János Magyar, Tamás Bányász, Péter P. Nánási
Dátum:2004
ISSN:1570-1611 (Linking)
Megjegyzések:The predominant isoform of the endothelin peptide family. endothelin-1 (ET-1)exerts various biological effects. These include effects on arterial smoothmuscle cells causing intense vasoconstriction and stimulation of cardiac cells.ET-1 promotes changes in cardiomyocytes that are consistent with electricalremodelling such as changes in ionic current density and inhomogeneousprolongation of action potential duration resulting in increased dispersion. Asfor the underlying mechanisms, ET-1 was shown to suppress several cAMP-dependentionic currents, such as ICa, IK and ICl in various mammalian cardiac preparationsincluding human myocytes; however, the degree of suppression of these currents isdifferent and highly dependent on experimental conditions. The proposedarrhythmogenic effects of ET-1 may also involve enhancement of Ca2+ release fromintracellular stores, generation of IP3, and acidosis due to stimulation of theNa+/H+ exchange. Furthermore, ET-1 acts as the natural counterpart toendothelium-derived nitric oxide, which exerts vasodilator, antithrombotic andantiproliferative effects, and inhibits leukocyte adhesion to the vascular wall.Effects of ET-1 are mediated through interaction with two major types of cellsurface receptors. ETA receptors have been associated with electricalremodelling, vasoconstriction and cell growth, while ETB receptors are involvedin the clearance of ET-1, inhibition of endothelial apoptosis, release of NO andprostacyclins, and inhibition of the expression of ET-1 converting enzyme. Thederangement of endothelial function in various cardiovascular diseases, such ascardiomyopathies, hypertension or arteriosclerosis, is a crucial element of thepathomechanism, thus ET receptors are considered as important therapeutictargets. Indeed, ET receptor antagonists may be able to preserve or restoreendothelial integrity and may have antiarrhythmic properties; therefore, they arepromising tools in cardiovascular medicine.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
0 (Endothelin-1)
0 (Endothelins)
0 (Protein Isoforms)
0 (Receptors, Endothelin)
7440-70-2 (Calcium)
Animals
Calcium/*metabolism
Electric Stimulation
Endothelin-1/adverse effects/metabolism/physiology
Endothelins/antagonists & inhibitors/biosynthesis/physiology
Humans
Muscle, Smooth, Vascular/drug effects/metabolism/physiology
Myocardial Contraction/drug effects/physiology
Myocytes, Cardiac/drug effects/metabolism
Protein Isoforms
Receptors, Endothelin/antagonists & inhibitors
Signal Transduction/drug effects
Vasoconstriction/drug effects/physiology
Ventricular Fibrillation/drug therapy
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current vascular pharmacology. - 2 : 1 (2004), p. 53-63. -
További szerzők:Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM081578
035-os BibID:(PMID)30963976
Első szerző:Muscogiuri, Giovanna
Cím:Calcium and Vitamin D Supplementation : myths and Realities with Regard to Cardiovascular Risk / Giovanna Muscogiuri, Luigi Barrea, Barbara Altieri, Carolina Di Somma, Harjit Pal Bhattoa, Daniela Laudisio, Guillaume T. Duval, Gabriella Pugliese, Cédric Annweiler, Francesco Orio, Hana Fakhouri, Silvia Savastano, Annamaria Colao
Dátum:2019
ISSN:1570-1611
Megjegyzések:Vitamin D and calcium are considered crucial for the treatment of bone diseases. Both vitamin D and calcium contribute to bone homeostasis but also preserve muscle health by reducing the risk of falls and fractures. Low vitamin D concentrations result in secondary hyperparathyroidism and contribute to bone loss, although the development of secondary hyperparathyroidism varies, even in patients with severe vitamin D deficiency. Findings from observational studies have shown controversial results regarding the association between bone mineral density and vitamin D/calcium status, thus sparking a debate regarding optimum concentrations of 25-hydroxyvitamin D and calcium for the best possible skeletal health. Although most of the intervention studies reported a positive effect of supplementation with calcium and vitamin D on bone in patients with osteoporosis, this therapeutic approach has been a matter of debate regarding potential side effects on the cardiovascular (CV) system. Thus, the aim of this review is to consider the current evidence on the physiological role of vitamin D and calcium on bone and muscle health. Moreover, we provide an overview on observational and interventional studies that investigate the effect of vitamin D and calcium supplementation on bone health, also taking into account the possible CV side-effects. We also provide molecular insights on the effect of calcium plus vitamin D on the CV system.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Vitamin D
bone health
calcium
cardiovascular system
myocardial infarction
stroke
Megjelenés:Current Vascular Pharmacology. - 17 : 6 (2019), p. 610-617. -
További szerzők:Barrea, Luigi Altieri, Barbara Di Somma, Carolina Bhattoa Harjit Pal (1973-) (laboratóriumi szakorvos) Laudisio, Daniela Duval, Guillaume Pugliese, Gabriella Annweiler, Cedric Orio, Francesco Fakhoury, Hana M. A. Savastano, Silvia Colao, Annamaria
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM007124
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Angiogenesis and its targeting in rheumatoid arthritis / Szekanecz, Z., Koch, A. E.
Dátum:2009
ISSN:1537-1891 (Print)
Megjegyzések:Angiogenesis, the development of new capillaries, is involved in leukocyte ingress into the synovium during the development and progression of rheumatoid arthritis. Several soluble and cell surface-bound mediators including growth factors, cytokines, chemokines, proteolytic matrix-degrading enzymes, cell adhesion molecules and others may promote synovial neovascularization. On the other hand, endogenous angiostatic factors, such as angiostatin, endostatin, interleukin-4 (IL-4), IL-13, interferons and some angiostatic chemokines are also produced within the rheumatoid synovium, however, their effects are insufficient to control synovial angiogenesis and inflammation. Several specific and non-specific strategies have been developed to block the action of angiogenic mediators. The first line of angiostatic agents include vascular endothelial growth factor (VEGF), angiopoietin, alpha(V)beta(3) integrin antagonist, as well as non-specific angiogenesis inhibitors including traditional disease-modifying agents (DMARDs), anti-tumor necrosis factor biologics, angiostatin, endostatin, fumagillin analogues or thalidomide. Potentially any angiostatic compound could be introduced to studies using animal models of arthritis or even to human rheumatoid arthritis trials.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Vascular Pharmacology. - 51 : 1 (2009), p. 1-7. -
További szerzők:Koch, Alisa E.
Internet cím:elektronikus változat
elektronikus változat
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6.

001-es BibID:BIBFORM003605
Első szerző:Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:Structure and function of poly(ADP-ribose) polymerase-1 : role in oxidative stress-related pathologies / Virág L.
Dátum:2005
Megjegyzések:Poly(ADP-ribosyl) ation is a reversible post-translational protein modification implicated in the regulation of a number of biological functions. Whereas an 18 member superfamily of poly(ADP-ribose) polymerase (PARP) enzymes synthesize poly(ADP-ribose) (PAR), a single protein, PAR glycohydrolase (PARG) is responsible for the catabolism of the polymer. PARP-1 accounts for more than 90% of the poly(ADP-ribosyl)ating capacity of the cells. PARP-1 activated by DNA breaks cleaves NAD(+) into nicotinamide and ADP-ribose and uses the latter to synthesize long branching PAR polymers covalently attached to acceptor proteins including histones, DNA repair enzymes, transcription factors and PARP-1. Whereas activation of PARP-1 by mild genotoxic stimuli may facilitate DNA repair and cell survival, irreparable DNA damage triggers apoptotic or necrotic cell death. In apoptosis, early PARP activation may assist the apoptotic cascade [e.g. by stabilizing p53, by mediating the translocation of apoptosis inducing factor (AIF) from the mitochondria to the nucleus or by inhibiting early activation of DNases]. In most severe oxidative stress situations, excessive DNA damage causes over activation of PARP-1, which incapacitates the apoptotic machinery and switches the mode of cell death from apoptosis to necrosis. Besides serving as a cytotoxic mediator, PARP-1 is also involved in transcriptional regulation, most notably in the NF kappaB and AP-1 driven expression of inflammatory mediators. Pharmacological inhibition or genetic ablation of PARP-1 provided remarkable protection from tissue injury in various oxidative stress-related disease models ranging from stroke, diabetes, diabetic endothelial dysfunction, myocardial ischemia-reperfusion, shock, Parkinson's disease, arthritis, colitis to dermatitis and uveitis. These beneficial effects are attributed to inhibition of the PARP-1 mediated suicidal pathway and to reduced expression of inflammatory cytokines and other mediators (e.g. inducible nitric oxide synthase).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
poly(ADP-ribose) polymerase
cytotoxicity
necrosis
apoptosis
DNA damage
peroxynitrite
Megjelenés:Current Vascular Pharmacology. - 3 : 3 (2005), p. 209-214. -
Internet cím:elektronikus változat
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