@article{MTMT:34691003,
	title = {17-Oxime ethers of oxidized ecdysteroid derivatives modulate oxidative stress in human brain endothelial cells and dose-dependently might protect or damage the blood-brain barrier},
	url = {https://m2.mtmt.hu/api/publication/34691003},
	author = {Vágvölgyi, Máté and Laczkó, Dávid and Santa Maria, Anaraquel and Vigh, Judit Piroska and Walter, Fruzsina and Berkecz, Róbert and Deli, Mária Anna and Tóth, Gábor and Hunyadi, Attila},
	doi = {10.1371/journal.pone.0290526},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {19},
	unique-id = {34691003},
	issn = {1932-6203},
	abstract = {20-Hydroxyecdysone and several of its oxidized derivatives exert cytoprotective effect in mammals including humans. Inspired by this bioactivity of ecdysteroids, in the current study it was our aim to prepare a set of sidechain-modified derivatives and to evaluate their potential to protect the blood-brain barrier (BBB) from oxidative stress. Six novel ecdysteroids, including an oxime and five oxime ethers, were obtained through regioselective synthesis from a sidechain-cleaved calonysterone derivative 2 and fully characterized by comprehensive NMR techniques revealing their complete 1 H and 13 C signal assignments. Surprisingly, several compounds sensitized hCMEC/D3 brain microvascular endothelial cells to tert -butyl hydroperoxide (tBHP)-induced oxidative damage as recorded by impedance measurements. Compound 8 , containing a benzyloxime ether moiety in its sidechain, was the only one that exerted a protective effect at a higher, 10 μM concentration, while at lower (10 nM– 1 μM) concentrations it promoted tBHP-induced cellular damage. Brain endothelial cells were protected from tBHP-induced barrier integrity decrease by treatment with 10 μM of compound 8 , which also mitigated the intracellular reactive oxygen species production elevated by tBHP. Based on our results, 17-oxime ethers of oxidized ecdysteroids modulate oxidative stress of the BBB in a way that may point towards unexpected toxicity. Further studies are needed to evaluate any possible risk connected to dietary ecdysteroid consumption and CNS pathologies in which BBB damage plays an important role.},
	year = {2024},
	eissn = {1932-6203},
	orcid-numbers = {Vágvölgyi, Máté/0000-0002-2233-9422; Santa Maria, Anaraquel/0000-0003-3505-5477; Walter, Fruzsina/0000-0001-8145-2823; Berkecz, Róbert/0000-0002-9076-2177; Deli, Mária Anna/0000-0001-6084-6524; Hunyadi, Attila/0000-0003-0074-3472}
}

@article{MTMT:34473973,
	title = {Nogo-A is secreted in extracellular vesicles, occurs in blood and can influence vascular permeability},
	url = {https://m2.mtmt.hu/api/publication/34473973},
	author = {Rust, Ruslan and Holm, Mea M. and Egger, Matteo and Weinmann, Oliver and van, Rossum Danielle and Walter, Fruzsina and Santa Maria, Anaraquel and Gronnert, Lisa and Maurer, Michael A. and Kraler, Simon and Akhmedov, Alexander and Cideciyan, Rose and Luscher, Thomas F. and Deli, Mária Anna and Herrmann, Inge K. and Schwab, Martin E.},
	doi = {10.1177/0271678X231216270},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	unique-id = {34473973},
	issn = {0271-678X},
	abstract = {Nogo-A is a transmembrane protein with multiple functions in the central nervous system (CNS), including restriction of neurite growth and synaptic plasticity. Thus far, Nogo-A has been predominantly considered a cell contact-dependent ligand signaling via cell surface receptors. Here, we show that Nogo-A can be secreted by cultured cells of neuronal and glial origin in association with extracellular vesicles (EVs). Neuron- and oligodendrocyte-derived Nogo-A containing EVs inhibited fibroblast spreading, and this effect was partially reversed by Nogo-A receptor S1PR2 blockage. EVs purified from HEK cells only inhibited fibroblast spreading upon Nogo-A over-expression. Nogo-A-containing EVs were found in vivo in the blood of healthy mice and rats, as well as in human plasma. Blood Nogo-A concentrations were elevated after acute stroke lesions in mice and rats. Nogo-A active peptides decreased barrier integrity in an in vitro blood-brain barrier model. Stroked mice showed increased dye permeability in peripheral organs when tested 2 weeks after injury. In the Miles assay, an in vivo test to assess leakage of the skin vasculature, a Nogo-A active peptide increased dye permeability. These findings suggest that blood borne, possibly EV-associated Nogo-A could exert long-range regulatory actions on vascular permeability.},
	keywords = {INHIBITION; NEURITE OUTGROWTH; PROTEINS; SYNAPTIC PLASTICITY; Hematology; Blood-Brain Barrier; stroke; Exosomes; Exosomes; nanoparticle tracking analysis; Endocrinology & Metabolism; axonal regeneration; BRAIN-BARRIER; Nogo-A; Corticospinal tract; S1PR2},
	year = {2024},
	eissn = {1559-7016},
	orcid-numbers = {Rust, Ruslan/0000-0003-3376-3453; Walter, Fruzsina/0000-0001-8145-2823; Santa Maria, Anaraquel/0000-0003-3505-5477; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:33688118,
	title = {Role of interleukin-6 and interleukin-10 in morphological and functional changes of the blood–brain barrier in hypertriglyceridemia},
	url = {https://m2.mtmt.hu/api/publication/33688118},
	author = {Barabási, Beáta and Barna, Lilla and Santa Maria, Anaraquel and Harazin, András and Molnár, Réka and Kincses, András and Vigh, Judit Piroska and Dukay, Brigitta and Sántha, Miklós and Tóth, Erzsébet Melinda and Walter, Fruzsina and Deli, Mária Anna and Hoyk, Zsófia},
	doi = {10.1186/s12987-023-00418-3},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {20},
	unique-id = {33688118},
	issn = {2045-8118},
	year = {2023},
	eissn = {2045-8118},
	orcid-numbers = {Santa Maria, Anaraquel/0000-0003-3505-5477; Harazin, András/0000-0002-0904-5606; Molnár, Réka/0000-0002-3128-825X; Walter, Fruzsina/0000-0001-8145-2823; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:33641697,
	title = {Highly Oxidized Ecdysteroids from a Commercial Cyanotis arachnoidea Root Extract as Potent Blood-Brain Barrier Protective Agents},
	url = {https://m2.mtmt.hu/api/publication/33641697},
	author = {Tóth, Gábor and Santa Maria, Anaraquel and Herke, Ibolya and Gáti, Tamás and Galvis-Montes, Daniel and Walter, Fruzsina and Deli, Mária Anna and Hunyadi, Attila},
	doi = {10.1021/acs.jnatprod.2c00948},
	journal-iso = {J NAT PROD},
	journal = {JOURNAL OF NATURAL PRODUCTS},
	volume = {86},
	unique-id = {33641697},
	issn = {0163-3864},
	year = {2023},
	eissn = {1520-6025},
	pages = {1074-1080},
	orcid-numbers = {Santa Maria, Anaraquel/0000-0003-3505-5477; Walter, Fruzsina/0000-0001-8145-2823; Deli, Mária Anna/0000-0001-6084-6524; Hunyadi, Attila/0000-0003-0074-3472}
}

@article{MTMT:32917592,
	title = {Effects of fasudil on blood-brain barrier integrity},
	url = {https://m2.mtmt.hu/api/publication/32917592},
	author = {Sato, Kei and Nakagawa, Shinsuke and Morofuji, Yoichi and Matsunaga, Yuki and Fujimoto, Takashi and Watanabe, Daisuke and Izumo, Tsuyoshi and Niwa, Masami and Walter, Fruzsina and Vigh, Judit Piroska and Santa Maria, Anaraquel and Deli, Mária Anna and Matsuo, Takayuki},
	doi = {10.1186/s12987-022-00336-w},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {19},
	unique-id = {32917592},
	issn = {2045-8118},
	abstract = {Background Cerebral infarction accounts for 85% of all stroke cases. Even in an era of rapid and effective recanalization using an intravascular approach, the majority of patients have poor functional outcomes. Thus, there is an urgent need for the development of therapeutic agents to treat acute ischemic stroke. We evaluated the effect of fasudil, a Rho kinase inhibitor, on blood brain barrier (BBB) functions under normoxia or oxygen-glucose deprivation (OGD) conditions using a primary cell-based in vitro BBB model. Methods BBB models from rat primary cultures (brain capillary endothelial cells, astrocytes, and pericytes) were subjected to either normoxia or 6 h OGD/24 h reoxygenation. To assess the effects of fasudil on BBB functions, we evaluated real time impedance, transendothelial electrical resistance (TEER), sodium fluorescein permeability, and tight junction protein expression using western blotting. Lastly, to understand the observed protective mechanism on BBB functions by fasudil we examined the role of cyclooxygenase-2 and thromboxane A2 receptor agonist U-46619 in BBB-forming cells. Results We found that treatment with 0.3-30 mu M of fasudil increased cellular impedance. Fasudil enhanced barrier properties in a concentration-dependent manner, as measured by an increased (TEER) and decreased permeability. Fasudil also increased the expression of tight junction protein claudin-5. Reductions in TEER and increased permeability were observed after OGD/reoxygenation exposure in mono- and co-culture models. The improvement in BBB integrity by fasudil was confirmed in both of the models, but was significantly higher in the co-culture than in the monoculture model. Treatment with U-46619 did not show significant changes in TEER in the monoculture model, whereas it showed a significant reduction in TEER in the co-culture model. Fasudil significantly improved the U-46619-induced TEER reduction in the co-culture models. Pericytes and astrocytes have opposite effects on endothelial cells and may contribute to endothelial injury in hyperacute ischemic stroke. Overall, fasudil protects the integrity of BBB both by a direct protective effect on endothelial cells and by a pathway mediated via pericytes and astrocytes. Conclusions Our findings suggest that fasudil is a BBB-protective agent against acute ischemic stroke.},
	keywords = {INHIBITION; CLEAVAGE; INJURY; ACTIVATION; ASTROCYTES; RHO-ASSOCIATED KINASE; Blood-Brain Barrier; ISCHEMIC-STROKE; tight junction; Thrombectomy; Acute ischemic stroke; pericytes; pericytes; fasudil; RHO-KINASE INHIBITOR; Oxygen-glucose deprivation-reoxygenation; CEREBRAL BARRIER},
	year = {2022},
	eissn = {2045-8118},
	orcid-numbers = {Morofuji, Yoichi/0000-0001-7135-2220; Walter, Fruzsina/0000-0001-8145-2823; Santa Maria, Anaraquel/0000-0003-3505-5477; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:32667372,
	title = {Blood–brain barrier dysfunction in l-ornithine induced acute pancreatitis in rats and the direct effect of l-ornithine on cultured brain endothelial cells},
	url = {https://m2.mtmt.hu/api/publication/32667372},
	author = {Walter, Fruzsina and Harazin, András and Tóth, Andrea and Veszelka, Szilvia and Santa Maria, Anaraquel and Barna, Lilla and Kincses, András and Biczo, G and Balla, Zsolt and Kui, Balázs and Maléth, József and Cervenak, László and Tubak, Vilmos and Kittel, Ágnes and Rakonczay, Zoltán and Deli, Mária Anna},
	doi = {10.1186/s12987-022-00308-0},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {19},
	unique-id = {32667372},
	issn = {2045-8118},
	year = {2022},
	eissn = {2045-8118},
	orcid-numbers = {Walter, Fruzsina/0000-0001-8145-2823; Harazin, András/0000-0002-0904-5606; Santa Maria, Anaraquel/0000-0003-3505-5477; Maléth, József/0000-0001-5768-3090; Cervenak, László/0000-0003-0166-8697; Tubak, Vilmos/0000-0002-6141-3920; Rakonczay, Zoltán/0000-0002-1499-3416; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:31642822,
	title = {Transport Studies Using Blood-Brain Barrier In Vitro Models. A Critical Review and Guidelines},
	url = {https://m2.mtmt.hu/api/publication/31642822},
	author = {Santa Maria, Anaraquel and Heymans, Marjolein and Walter, Fruzsina and Culot, Maxime and Gosselet, Fabien and Deli, Mária Anna and Neuhaus, Winfried},
	doi = {10.1007/164_2020_394},
	journal-iso = {HANDB EXP PHARMACOL},
	journal = {HANDBOOK OF EXPERIMENTAL PHARMACOLOGY},
	volume = {273},
	unique-id = {31642822},
	issn = {0171-2004},
	abstract = {Permeation is one of the most evaluated parameters using preclinical in vitro blood-brain barrier models, as it has long been considered to be one of the major factors influencing central nervous system drug delivery. Blood-brain barrier permeability can be defined as the speed at which a compound crosses the brain endothelial cell barrier and is employed to assess barrier tightness, which is a crucial feature of brain capillaries in vivo. In addition, it is used to assess brain drug penetration. We review traditionally used methods to assess blood-brain barrier permeability in vitro and summarize often neglected in vivo (e.g., plasma protein and brain tissue binding) or in vitro (e.g., culture insert materials or methodology) factors that influence this property. These factors are crucial to consider when performing BBB permeability assessments, and especially when comparing permeability data obtained from different models, since model diversification significantly complicates inter-study comparisons. Finally, measuring transendothelial electrical resistance can be used to describe blood-brain barrier tightness; however, several parameters should be considered while comparing these measurements to the blood-brain barrier permeability to paracellular markers.},
	keywords = {drug transport; penetration; brain capillary endothelial cells; TEER; Paracellular transport; Cell layer tightness},
	year = {2022},
	pages = {187-204},
	orcid-numbers = {Santa Maria, Anaraquel/0000-0003-3505-5477; Walter, Fruzsina/0000-0001-8145-2823; Deli, Mária Anna/0000-0001-6084-6524}
}

@mastersthesis{MTMT:32473952,
	title = {The role of brain endothelial surface charge and glycocalyx in the function and integrity of the blood-brain barrier [Az agyi endotélsejtek sejtfelszíni töltésének és glikokalix rétegének szerepe a vér-agy gát integritásában és működésében]},
	url = {https://m2.mtmt.hu/api/publication/32473952},
	author = {Santa Maria, Anaraquel},
	doi = {10.14232/phd.10751},
	publisher = {SZTE},
	unique-id = {32473952},
	year = {2021},
	orcid-numbers = {Santa Maria, Anaraquel/0000-0003-3505-5477}
}

@article{MTMT:32156171,
	title = {MAP Kinase Pathways in Brain Endothelial Cells and Crosstalk with Pericytes and Astrocytes Mediate Contrast-Induced Blood–Brain Barrier Disruption},
	url = {https://m2.mtmt.hu/api/publication/32156171},
	author = {Matsunaga, Yuki and Nakagawa, Shinsuke and Morofuji, Yoichi and Dohgu, Shinya and Watanabe, Daisuke and Horie, Nobutaka and Izumo, Tsuyoshi and Niwa, Masami and Walter, Fruzsina and Santa Maria, Anaraquel and Deli, Mária Anna and Matsuo, Takayuki},
	doi = {10.3390/pharmaceutics13081272},
	journal-iso = {PHARMACEUTICS},
	journal = {PHARMACEUTICS},
	volume = {13},
	unique-id = {32156171},
	issn = {1999-4923},
	year = {2021},
	eissn = {1999-4923},
	orcid-numbers = {Morofuji, Yoichi/0000-0001-7135-2220; Dohgu, Shinya/0000-0002-8036-0510; Niwa, Masami/0000-0001-5138-5180; Walter, Fruzsina/0000-0001-8145-2823; Santa Maria, Anaraquel/0000-0003-3505-5477; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:32077894,
	title = {Transendothelial Electrical Resistance Measurement across the Blood–Brain Barrier: A Critical Review of Methods},
	url = {https://m2.mtmt.hu/api/publication/32077894},
	author = {Vigh, Judit Piroska and Kincses, András and Ozgür, Burak and Walter, Fruzsina and Santa Maria, Anaraquel and Valkai, Sándor and Vastag, Monika and Neuhaus, Winfried and Brodin, Birger and Dér, András and Deli, Mária Anna},
	doi = {10.3390/mi12060685},
	journal-iso = {MICROMACHINES-BASEL},
	journal = {MICROMACHINES},
	volume = {12},
	unique-id = {32077894},
	year = {2021},
	eissn = {2072-666X},
	orcid-numbers = {Walter, Fruzsina/0000-0001-8145-2823; Santa Maria, Anaraquel/0000-0003-3505-5477; Valkai, Sándor/0000-0001-8479-8141; Neuhaus, Winfried/0000-0002-6552-7183; Deli, Mária Anna/0000-0001-6084-6524}
}