@article{MTMT:30734491,
	title = {Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury : protective effects of the mitochondria-targeted antioxidative peptide SS-31},
	url = {https://m2.mtmt.hu/api/publication/30734491},
	author = {Czigler, András and Tóth, Luca and Szarka, Nikolett and Berta, Gergely and Amrein, Krisztina and Czeiter, Endre and Lendvai-Emmert, Dominika and Bodó, Kornélia and Tarantini, Stefano and Koller, Ákos and Ungvári, Zoltán István and Büki, András and Tóth, Péter József},
	doi = {10.1089/neu.2019.6439},
	journal-iso = {J NEUROTRAUM},
	journal = {JOURNAL OF NEUROTRAUMA},
	volume = {36},
	unique-id = {30734491},
	issn = {0897-7151},
	abstract = {Traumatic brain injury (TBI) induces cerebrovascular oxidative stress, which is associated with neurovascular uncoupling, autoregulatory dysfunction and persisting cognitive decline in both preclinical models and patients. However, single mild TBI, the most frequent form of brain trauma increases cerebral generation of reactive oxygen species (ROS) only transiently. We hypothesized, that co-morbid conditions may exacerbate long term ROS generation in cerebral arteries after mTBI. Since hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive and spontaneously hypertensive rats (SHR) and assessed changes in cytoplasmic and mitochondrial superoxide (O2-) production by confocal microscopy in isolated middle cerebral arteries (MCA) two weeks after mTBI using dihydroethidine (DHE) and the mitochondria-targeted redox sensitive fluorescent indicator dye MitoSox. We found that mTBI induced a significant increase in long term cytoplasmic and mitochondrial O2- production in MCAs of SHRs and increased expression of the NADPH oxidase subunit Nox4, which were reversed to the normal level by treating the animals with the cell-permeable, mitochondria-targeted antioxidant peptide SS-31(5.7 mg kg-1 day-1 , i.p.). Persistent mTBI-induced oxidative stress in MCAs of SHRs was significantly decreased by inhibiting vascular NADPH oxidase (apocyinin). We propose, that hypertension- and mTBI-induced cerebrovascular oxidative stress likely lead to persistent dysregulation of CBF and cognitive dysfunction, which might be reversed by SS-31 treatment.},
	keywords = {antioxidants; Mitochondria; RADICAL SCAVENGERS; confocal microscopy; Oxidative stress},
	year = {2019},
	eissn = {1557-9042},
	pages = {3309-3315},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944; Tarantini, Stefano/0000-0001-5627-1430; Koller, Ákos/0000-0003-3256-8701; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30413407,
	title = {VPAC1 receptors play a dominant role in PACAP-induced vasorelaxation in female mice},
	url = {https://m2.mtmt.hu/api/publication/30413407},
	author = {Ivic, Ivan and Balaskó, Márta and Fülöp, Balázs Dániel and Hashimoto, Hitoshi and Tóth, Gábor and Tamás, Andrea and Juhász, Tamás and Koller, Ákos and Reglődi, Dóra and Varjú-Solymár, Margit},
	doi = {10.1371/journal.pone.0211433},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {14},
	unique-id = {30413407},
	issn = {1932-6203},
	abstract = {PACAP and VIP are closely related neuropeptides with wide distribution and potent effect in the vasculature. We previously reported vasomotor activity in peripheral vasculature of male wild type (WT) and PACAP-deficient (KO) mice. However, female vascular responses are still unexplored. We hypothesized that PACAP-like activity is maintained in female PACAP KO mice and the mechanism through which it is regulated differs from that of male PACAP KO animals.We investigated the vasomotor effects of VIP and PACAP isoforms and their selective blockers in WT and PACAP KO female mice in carotid and femoral arteries. The expression and level of different PACAP receptors in the vessels were measured by RT-PCR and Western blot.In both carotid and femoral arteries of WT mice, PACAP1-38, PACAP1-27 or VIP induced relaxation, without pronounced differences between them. Reduced relaxation was recorded only in the carotid arteries of KO mice as compared to their WT controls. The specific VPAC1R antagonist completely blocked the PACAP/VIP-induced relaxation in both arteries of all mice, while PAC1R antagonist affected relaxation only in their femoral arteries.In female WT mice, VPAC1 receptors appear to play a dominant role in PACAP-induced vasorelaxation both in carotid and in femoral arteries. In the PACAP KO group PAC1R activation exerts vasorelaxation in the femoral arteries but in carotid arteries there is no significant effect of the activation of this receptor. In the background of this regional difference, decreased PAC1R and increased VPAC1R availability in the carotid arteries was found.},
	year = {2019},
	eissn = {1932-6203},
	orcid-numbers = {Tóth, Gábor/0000-0002-3604-4385; Koller, Ákos/0000-0003-3256-8701; Varjú-Solymár, Margit/0000-0001-6667-6263}
}

@article{MTMT:33192843,
	title = {Emlékezés Dr. John O. Holloszy professzorra. Remembering Dr. John O. Holloszy},
	url = {https://m2.mtmt.hu/api/publication/33192843},
	author = {Nemerkényiné Hidegkuti, Krisztina and Koller, Ákos},
	journal-iso = {TESTNEVELÉS SPORT TUDOMÁNY},
	journal = {TESTNEVELÉS SPORT TUDOMÁNY / PHYSICAL EDUCATION, SPORT, SCIENCE},
	volume = {3},
	unique-id = {33192843},
	issn = {2498-7646},
	year = {2018},
	eissn = {2560-0346},
	pages = {64-65},
	orcid-numbers = {Koller, Ákos/0000-0003-3256-8701}
}

@article{MTMT:30397629,
	title = {Négy hetes napi futás-tréning a patkány szívkoszorúserek biomechanikai és funkcionális adaptációját hozza létre},
	url = {https://m2.mtmt.hu/api/publication/30397629},
	author = {Koller, Ákos and Nádasy, György László and Bednárikné Dörnyei, Gabriella and Szénási, Annamária and Szekeres, Mária},
	journal-iso = {M SPORTTUD SZLE},
	journal = {MAGYAR SPORTTUDOMÁNYI SZEMLE},
	volume = {19},
	unique-id = {30397629},
	issn = {1586-5428},
	year = {2018},
	pages = {55-56},
	orcid-numbers = {Koller, Ákos/0000-0003-3256-8701; Nádasy, György László/0000-0003-2057-2391; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Szénási, Annamária/0000-0002-2422-1081; Szekeres, Mária/0000-0002-6358-7270}
}

@article{MTMT:3393140,
	title = {Coronary microvascular and cardiac dysfunction due to homocysteine pathometabolism; a complex therapeutic design},
	url = {https://m2.mtmt.hu/api/publication/3393140},
	author = {Koller, Ákos and Szénási, Annamária and Bednárikné Dörnyei, Gabriella and Kovacs, N and Lelbach, Ádám Antal and Kovacs, I},
	doi = {10.2174/1381612824666180625125450},
	journal-iso = {CURR PHARM DESIGN},
	journal = {CURRENT PHARMACEUTICAL DESIGN},
	volume = {24},
	unique-id = {3393140},
	issn = {1381-6128},
	abstract = {In various metabolic diseases both the coronary circulation and cardiac metabolism are altered. Here we summarize the effects of a condition called hyperhomocysteinemia (HHcy) - which can develop due to genetic or environmental causes - on the function of coronary microvessels and heart. This metabolic disease is underappreciated, yet even mild or moderate elevation of plasma concentrations of homocystein (Hcy, plasma Hcy >16 M), a sulfur-containing amino acid produced via methionine metabolism) leads to coronary and peripheral artery and even venous vessel diseases, leading to vasomotor dysfunction and increased thrombosis, consequently increased morbidity and mortality. Yet the underlying mechanisms are not yet revealed. Recent studies indicated that there are common pathomechanisms, which may affect all cellular function involved. Two main mechanisms are the dysfunction of nitric oxide (NO) pathway resulting reduced dilator responses of arteries and arterioles with methionine diet-induced hyperhomocysteinemia, and the simultaneously increased thromboxane A2 (TXA2) activity both in vessels and platelets. These changes are likely due to an increased production of reactive oxidative species (oxidative stress) due to increased NADPH oxidase assembly, which eventually lead to inflammatory process (indicated by increases in TNFalpha, NFkappabeta, p22phox, p67phox, and rac-1, levels) and changes in various gene expressions and morphological remodeling of vessels. Increased superoxide production and reduced ability of NO alters the regulation of mitochondrial function in the myocardium. The interactions of these pathomechanisms may explain why HHcy increases the uptake of glucose and lactate and decreases the uptake of free fatty acid by the heart. The pathological consequences of HHcy could be worsening by the simultaneous presence of other risk factors, such as hyperlipidemia, diabetes mellitus and metabolic syndrome. All in all, HHcy and associated pathometabolism lead to severe changes and dysfunctions of coronary arterial vessels and cardiac function, which may not always apparent in clinical settings but most likely, contribute to increased prevalence of cardiovascular diseases and mortality, which however can be reduced by appropriate prevention and treatments. We believe that HHcy is an underestimated - likely due to inappropriate clinical trials - but serious disease condition because it promotes the development of atherosclerosis in large arterial vessels, vasomotor dysfunction in microvessels, hypertension and thrombosis. In this review we will summarizes previous functional findings focusing on coronary vessels and cardiac function and the underlying cellular and molecular mechanisms enabling the development of novel treatments.},
	year = {2018},
	eissn = {1873-4286},
	pages = {2911-2920},
	orcid-numbers = {Koller, Ákos/0000-0003-3256-8701; Szénási, Annamária/0000-0002-2422-1081; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252}
}

@article{MTMT:3360066,
	title = {Extravascular Blood Augments Myogenic Constriction of Cerebral Arterioles: Implications for Hemorrhage-Induced Vasospasm.},
	url = {https://m2.mtmt.hu/api/publication/3360066},
	author = {Deng, W and Kandhi, S and Zhang, B and Huang, A and Koller, Ákos and Sun, D},
	doi = {10.1161/JAHA.118.008623},
	journal-iso = {J AM HEART ASSOC},
	journal = {JOURNAL OF THE AMERICAN HEART ASSOCIATION},
	volume = {7},
	unique-id = {3360066},
	issn = {2047-9980},
	abstract = {BACKGROUND: Subarachnoid hemorrhage is a serious clinical condition that impairs local cerebral blood flow perfusion and consequently initiates neuronal dysfunction. Pressure-sensitive myogenic vasomotor regulation is an important mechanism involved in the regulation of cerebral blood flow. We hypothesized that extravascular hemolyzed blood enhances arteriolar myogenic constriction, which in vivo may contribute to the reduction of local cerebral blood flow after subarachnoid hemorrhage. METHODS AND RESULTS: Arterioles isolated from the middle cerebral artery (MCA arterioles) of mice were cannulated in a perfusion chamber. Arteriolar diameters in response to step increases in intraluminal pressure (20-120 mm Hg) were measured in various experimental conditions. In response to increases in intraluminal pressure, all MCA arterioles exhibited myogenic vasoconstrictions. Compared with controls, the pressure-induced constriction was significantly enhanced in arterioles (in vitro) exposed to extravascular hemolyzed blood or different concentrations of extracellular erythrocyte lysate (1%, 10%, and 20%) for different exposure durations (1-6 hours). The magnitude of enhancement was proportional to the lysate concentration and exposure duration. In in vivo experiments, 10 muL of autologous blood lysate were injected into the mouse subarachnoid space on the surface of the left MCA. Two hours later, MCA arterioles were isolated and left MCA arterioles displayed enhanced myogenic responses compared with the right MCA. The enhanced myogenic response was prevented by scavenge of superoxide in both in vitro and in vivo experiments. CONCLUSIONS: Extravascular hemolyzed blood, perhaps by promoting vascular production of superoxide, augments myogenic constriction of cerebral arterioles, which plays a crucial role in the subarachnoid hemorrhage-induced cerebral ischemia.},
	keywords = {DYSFUNCTION; NITRIC-OXIDE; PRESSURE; MICROCIRCULATION; SUBARACHNOID HEMORRHAGE; SUBARACHNOID HEMORRHAGE; AUTOREGULATION; MYOGENIC RESPONSE; afferent arteriole; Intracerebral hemorrhage; SUPEROXIDE-PRODUCTION; cerebral arterioles; Oxidative stress},
	year = {2018},
	eissn = {2047-9980},
	orcid-numbers = {Koller, Ákos/0000-0003-3256-8701}
}

@article{MTMT:3294542,
	title = {Aging-Induced Modulation of Pituitary Adenylate Cyclase-Activating Peptide- and Vasoactive Intestinal Peptide-Induced Vasomotor Responses in the Arteries of Mice},
	url = {https://m2.mtmt.hu/api/publication/3294542},
	author = {Ivic, Ivan and Varjú-Solymár, Margit and Fülöp, Balázs Dániel and Hashimoto, H and Tóth, Gábor and Tamás, Andrea and Juhász, Tamás and Koller, Ákos and Reglődi, Dóra},
	doi = {10.1159/000481781},
	journal-iso = {J VASC RES},
	journal = {JOURNAL OF VASCULAR RESEARCH},
	volume = {54},
	unique-id = {3294542},
	issn = {1018-1172},
	abstract = {Pituitary adenylate cyclase-activating peptide (PACAP; 1-38 and 1-27) and vasoactive intestinal peptide (VIP) are related neuropeptides of the secretin/glucagon family. Overlapping signaling through G-protein-coupled receptors mediates their vasomotor activity. We previously showed that PACAP deficiency (PACAP-KO) shifts the mechanisms of vascular response and maintains arterial relaxation through the VIP backup mechanism and (mainly) its VPAC1R, but their age-dependent modulation is still unknown. We hypothesized that backup mechanisms exist, which maintain the vasomotor activity of these peptides also in older age. Thus, we investigated the effects of exogenous VIP and PACAP peptides in isolated carotid arteries of 2- and 15-month-old wild-type (WT) and PACAP-KO mice. All peptides induced relaxation in the arteries of young WT mice, whereas in young PACAP-KO mice PACAP1-27 and VIP, but not PACAP1-38, induced relaxation. Unlike VIP, PACAP-induced vasomotor responses were reduced in aging WT mice. However, in the arteries of aging PACAP-KO mice, PACAP1-27- and VIP-induced responses were reduced, but PACAP1-38 showed a greater vasomotor response compared to that of young PACAP-KO animals. There were no significant differences between the vasomotor responses of aging WT and PACAP-KO mice. Our data suggest that, in the absence of PACAP both in young and old ages, the vascular response is mediated through backup mechanisms, most likely VIP, maintaining proper vascular relaxation in aging-induced PACAP insufficiency.},
	year = {2017},
	eissn = {1423-0135},
	pages = {359-366},
	orcid-numbers = {Varjú-Solymár, Margit/0000-0001-6667-6263; Tóth, Gábor/0000-0002-3604-4385; Koller, Ákos/0000-0003-3256-8701}
}

@article{MTMT:3145593,
	title = {Új low back pain prevenciós mozgásprogram, amely javítja a törzsizmok állapotát és a lumbalis motoros kontrollt [Improvement of lumbal motor control and trunkmuscle conditions with a novel low back pain prevention exercise program]},
	url = {https://m2.mtmt.hu/api/publication/3145593},
	author = {Kovácsné Bobály, Viktória and Szilágyi, Brigitta and Makai, Alexandra and Koller, Ákos and Járomi, Melinda},
	doi = {10.1556/650.2017.30640},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {158},
	unique-id = {3145593},
	issn = {0030-6002},
	year = {2017},
	eissn = {1788-6120},
	pages = {58-66},
	orcid-numbers = {Makai, Alexandra/0000-0002-1907-120X; Koller, Ákos/0000-0003-3256-8701}
}

@article{MTMT:3066227,
	title = {Vázizomkisvénák vazomotortónusának intrinszik szabályozómechanizmusai},
	url = {https://m2.mtmt.hu/api/publication/3066227},
	author = {Szénási, Annamária and Bednárikné Dörnyei, Gabriella and Racz, A and Debreczeni, Béla and Koller, Ákos},
	doi = {10.1556/650.2016.30461},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {157},
	unique-id = {3066227},
	issn = {0030-6002},
	abstract = {In many developed countries the prevalence of venous disorders and its consequences are higher than that of arterial diseases. Thus it is very important to understand the exact physiological and pathophysiological function of small veins and their control mechanisms. Small veins and venules have an important role in the regulation of capillary fluid exchange, as well as return of the venous blood into the heart. However, there is only limited knowledge available regarding the role of local mechanisms controlling the vasomotor tone and diameter of small veins. In the last decade the authors focused on the elucidation of these mechanisms in isolated skeletal muscle venules of rats. Their results suggest that the tone of small veins is controlled by the integration of several mechanisms, activated by the intraluminal pressure and flow/wall shear stress, in addition to numerous local mediators synthesized and released from the smooth muscle and endothelium. These mechanisms are involved - in a complex manner - in the control of postcapillary resistance, thus regulation of tissue blood supply, venous return and consequently in the modulation of the cardiac output, as well. Orv. Hetil., 2016, 157(21), 805-812.},
	year = {2016},
	eissn = {1788-6120},
	pages = {805-812},
	orcid-numbers = {Szénási, Annamária/0000-0002-2422-1081; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Koller, Ákos/0000-0003-3256-8701}
}