@article{MTMT:34720930,
	title = {A “torn bag mechanism” of small extracellular vesicle release via limiting membrane rupture of en bloc released amphisomes (amphiectosomes)},
	url = {https://m2.mtmt.hu/api/publication/34720930},
	author = {Visnovitz, Tamás and Lenzinger, Dorina and Koncz, Anna and Vizi, Péter Márk and Bárkai, Tünde and Visnovitzné Dr Vukman, Krisztina and Galinsoga, Alicia and Németh, Krisztina and Fletcher, Kelsey Aine and Komlósi, Zsolt and Cserép, Csaba and Dénes, Ádám and Lőrincz, Péter and Valcz, Gábor and Buzás, Edit Irén},
	doi = {10.7554/eLife.95828.3},
	journal-iso = {ELIFE},
	journal = {ELIFE},
	volume = {13},
	unique-id = {34720930},
	issn = {2050-084X},
	abstract = {Recent studies showed an unexpected complexity of extracellular vesicle (EV) biogenesis pathways. We previously found evidence that human colorectal cancer cells in vivo release large multivesicular body-like structures en bloc. Here, we tested whether this large EV type is unique to colorectal cancer cells. We found that all cell types we studied (including different cell lines and cells in their original tissue environment) released multivesicular large EVs (MV-lEVs). We also demonstrated that upon spontaneous rupture of the limiting membrane of the MV-lEVs, their intraluminal vesicles (ILVs) escaped to the extracellular environment by a ‘torn bag mechanism’. We proved that the MV-lEVs were released by ectocytosis of amphisomes (hence, we termed them amphiectosomes). Both ILVs of amphiectosomes and small EVs separated from conditioned media were either exclusively CD63 or LC3B positive. According to our model, upon fusion of multivesicular bodies with autophagosomes, fragments of the autophagosomal inner membrane curl up to form LC3B positive ILVs of amphisomes, while CD63 positive small EVs are of multivesicular body origin. Our data suggest a novel common release mechanism for small EVs, distinct from the exocytosis of multivesicular bodies or amphisomes, as well as the small ectosome release pathway.},
	year = {2025},
	eissn = {2050-084X},
	orcid-numbers = {Visnovitz, Tamás/0000-0002-7962-5083; Koncz, Anna/0000-0003-2511-2394; Németh, Krisztina/0000-0002-3825-2137; Fletcher, Kelsey Aine/0009-0001-1668-5222; Komlósi, Zsolt/0000-0002-4149-1497; Cserép, Csaba/0000-0001-5513-2471; Lőrincz, Péter/0000-0001-7374-667X; Valcz, Gábor/0000-0002-7109-3529; Buzás, Edit Irén/0000-0002-3744-206X}
}

@article{MTMT:35830704,
	title = {Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19},
	url = {https://m2.mtmt.hu/api/publication/35830704},
	author = {Fekete, Rebeka and Simats, Alba and Bíró, Eduárd and Pósfai, Balázs and Cserép, Csaba and Schwarcz, Dóra Anett and Cserépné Szabadits, Eszter and Környei, Zsuzsanna and Tóth, Krisztina and Fichó, Erzsébet and Szalma, János and Vida, Sára and Kellermayer, Anna and Dávid, Csaba and Acsády, László and Kontra, Levente and Silvestre-Roig, Carlos and Moldvay, Judit and Fillinger, János and Csikász-Nagy, Attila and Hortobágyi, Tibor and Liesz, Arthur and Benkő, Szilvia and Dénes, Ádám},
	doi = {10.1038/s41593-025-01871-z},
	journal-iso = {NAT NEUROSCI},
	journal = {NATURE NEUROSCIENCE},
	volume = {28},
	unique-id = {35830704},
	issn = {1097-6256},
	abstract = {COVID-19 is associated with diverse neurological abnormalities, but the underlying mechanisms are unclear. We hypothesized that microglia, the resident immune cells of the brain, are centrally involved in this process. To study this, we developed an autopsy platform allowing the integration of molecular anatomy, protein and mRNA datasets in postmortem mirror blocks of brain and peripheral organ samples from cases of COVID-19. We observed focal loss of microglial P2Y12R, CX3CR1–CX3CL1 axis deficits and metabolic failure at sites of virus-associated vascular inflammation in severely affected medullary autonomic nuclei and other brain areas. Microglial dysfunction is linked to mitochondrial injury at sites of excessive synapse and myelin phagocytosis and loss of glutamatergic terminals, in line with proteomic changes of synapse assembly, metabolism and neuronal injury. Furthermore, regionally heterogeneous microglial changes are associated with viral load and central and systemic inflammation related to interleukin (IL)-1 or IL-6 via virus-sensing pattern recognition receptors and inflammasomes. Thus, SARS-CoV-2-induced inflammation might lead to a primarily gliovascular failure in the brain, which could be a common contributor to diverse COVID-19-related neuropathologies.},
	keywords = {neuroimmunology; Diseases of the nervous system},
	year = {2025},
	eissn = {1546-1726},
	pages = {558-576},
	orcid-numbers = {Pósfai, Balázs/0000-0003-1035-565X; Cserép, Csaba/0000-0001-5513-2471; Fichó, Erzsébet/0000-0002-3965-8438; Csikász-Nagy, Attila/0000-0002-2919-5601; Hortobágyi, Tibor/0000-0001-5732-7942; Liesz, Arthur/0000-0002-9069-2594}
}

@article{MTMT:34350929,
	title = {Microglia–neuron–vascular interactions in ischemia},
	url = {https://m2.mtmt.hu/api/publication/34350929},
	author = {Lénárt, Nikolett and Cserép, Csaba and Császár, Eszter and Pósfai, Balázs and Dénes, Ádám},
	doi = {10.1002/glia.24487},
	journal-iso = {GLIA},
	journal = {GLIA},
	volume = {72},
	unique-id = {34350929},
	issn = {0894-1491},
	abstract = {Cerebral ischemia is a devastating condition that results in impaired blood flow in the brain leading to acute brain injury. As the most common form of stroke, occlusion of cerebral arteries leads to a characteristic sequence of pathophysiological changes in the brain tissue. The mechanisms involved, and comorbidities that determine outcome after an ischemic event appear to be highly heterogeneous. On their own, the processes leading to neuronal injury in the absence of sufficient blood supply to meet the metabolic demand of the cells are complex and manifest at different temporal and spatial scales. While the contribution of non‐neuronal cells to stroke pathophysiology is increasingly recognized, recent data show that microglia, the main immune cells of the central nervous system parenchyma, play previously unrecognized roles in basic physiological processes beyond their inflammatory functions, which markedly change during ischemic conditions. In this review, we aim to discuss some of the known microglia–neuron–vascular interactions assumed to contribute to the acute and delayed pathologies after cerebral ischemia. Because the mechanisms of neuronal injury have been extensively discussed in several excellent previous reviews, here we focus on some recently explored pathways that may directly or indirectly shape neuronal injury through microglia‐related actions. These discoveries suggest that modulating gliovascular processes in different forms of stroke and other neurological disorders might have presently unexplored therapeutic potential in combination with neuroprotective and flow restoration strategies.},
	year = {2024},
	eissn = {1098-1136},
	pages = {833-856},
	orcid-numbers = {Lénárt, Nikolett/0000-0002-7456-949X; Cserép, Csaba/0000-0001-5513-2471; Császár, Eszter/0000-0002-5543-4100; Pósfai, Balázs/0000-0003-1035-565X}
}

@article{MTMT:35058848,
	title = {Microglia contribute to neuronal synchrony despite endogenous ATP-related phenotypic transformation in acute mouse brain slices},
	url = {https://m2.mtmt.hu/api/publication/35058848},
	author = {Berki, Péter and Cserép, Csaba and Környei, Zsuzsanna and Pósfai, Balázs and Cserépné Szabadits, Eszter and Domonkos, Andor and Kellermayer, Anna and Nyerges, Miklós and Wei, Xiaofei and Mody, Istvan and Kunihiko, Araki and Beck, Heinz and Kaikai, He and Ya, Wang and Lénárt, Nikolett and Wu, Zhaofa and Jing, Miao and Li, Yulong and Gulyás, Attila and Dénes, Ádám},
	doi = {10.1038/s41467-024-49773-1},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {15},
	unique-id = {35058848},
	issn = {2041-1723},
	year = {2024},
	eissn = {2041-1723},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X; Lénárt, Nikolett/0000-0002-7456-949X; Gulyás, Attila/0000-0003-4961-636X}
}

@article{MTMT:35176925,
	title = {Microglia rescue neurons from aggregate-induced neuronal dysfunction and death through tunneling nanotubes},
	url = {https://m2.mtmt.hu/api/publication/35176925},
	author = {Scheiblich, H. and Eikens, F. and Wischhof, L. and Opitz, S. and Jüngling, K. and Cserép, Csaba and Schmidt, S.V. and Lambertz, J. and Bellande, T. and Pósfai, Balázs and Geck, C. and Spitzer, J. and Odainic, A. and Castro-Gomez, S. and Schwartz, S. and Boussaad, I. and Krüger, R. and Glaab, E. and Di, Monte D.A. and Bano, D. and Dénes, Ádám and Latz, E. and Melki, R. and Pape, H.-C. and Heneka, M.T.},
	doi = {10.1016/j.neuron.2024.06.029},
	journal-iso = {NEURON},
	journal = {NEURON},
	volume = {112},
	unique-id = {35176925},
	issn = {0896-6273},
	year = {2024},
	eissn = {1097-4199},
	pages = {3106-3125.e8},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X}
}

@article{MTMT:35257522,
	title = {Contactomics of Microglia and Intercellular Communication},
	url = {https://m2.mtmt.hu/api/publication/35257522},
	author = {Cserép, Csaba and Pósfai, Balázs and Cserépné Szabadits, Eszter and Dénes, Ádám},
	doi = {10.1007/978-3-031-55529-9_8},
	journal-iso = {ADVANCES IN NEUROBIOLOGY},
	journal = {ADVANCES IN NEUROBIOLOGY},
	volume = {37},
	unique-id = {35257522},
	issn = {2190-5215},
	year = {2024},
	eissn = {2190-5223},
	pages = {135-149},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X}
}

@article{MTMT:32636201,
	title = {The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner},
	url = {https://m2.mtmt.hu/api/publication/32636201},
	author = {Tóth, Krisztina and Lénárt, Nikolett and Berki, Péter and Fekete, Rebeka and Cserépné Szabadits, Eszter and Pósfai, Balázs and Cserép, Csaba and Alatshan, Ahmad and Benkő, Szilvia and Kiss, Dániel and Hübner, Christian A. and Gulyás, Attila and Kaila, Kai and Környei, Zsuzsanna and Dénes, Ádám},
	doi = {10.1371/journal.pbio.3001526},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {20},
	unique-id = {32636201},
	issn = {1544-9173},
	abstract = {The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has remained unclear to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology, process recruitment to the site of injury, and adaptation to changes in cellular volume in a cell-autonomous manner via regulating membrane conductance. In addition, microglial NKCC1 deficiency results in NLRP3 inflammasome priming and increased production of interleukin-1β (IL-1β), rendering microglia prone to exaggerated inflammatory responses. In line with this, central (intracortical) administration of the NKCC1 blocker, bumetanide, potentiated intracortical lipopolysaccharide (LPS)-induced cytokine levels. In contrast, systemic bumetanide application decreased inflammation in the brain. Microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema, and, worse, neurological outcome. Thus, NKCC1 emerges as an important player in controlling microglial ion homeostasis and inflammatory responses through which microglia modulate brain injury. The contribution of microglia to central NKCC1 actions is likely to be relevant for common neurological disorders.},
	keywords = {Inflammation; MICROGLIAL CELLS; Cytokines; SPLEEN; edema; brain damage; membrane potential; Intraperitoneal injections},
	year = {2022},
	eissn = {1545-7885},
	orcid-numbers = {Lénárt, Nikolett/0000-0002-7456-949X; Pósfai, Balázs/0000-0003-1035-565X; Cserép, Csaba/0000-0001-5513-2471; Kiss, Dániel/0000-0002-8482-8862; Gulyás, Attila/0000-0003-4961-636X; Kaila, Kai/0000-0003-0668-5955}
}

@article{MTMT:32710992,
	title = {Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions.},
	url = {https://m2.mtmt.hu/api/publication/32710992},
	author = {Császár, Eszter and Lénárt, Nikolett and Cserép, Csaba and Környei, Zsuzsanna and Fekete, Rebeka and Pósfai, Balázs and Balázsfi, Diána and Hangya, Balázs and Schwarcz, Dóra Anett and Cserépné Szabadits, Eszter and Szöllősi, Dávid and Szigeti, Krisztián and Máthé, Domokos and West, Brian L and Tóthné Sviatkó, Katalin and Brás, Ana Rita and Mariani, Jean-Charles and Kliewer, Andrea and Lenkei, Zsolt and Hricisák, László and Benyó, Zoltán and Baranyi, Mária and Sperlágh, Beáta and Menyhárt, Ákos and Farkas, Eszter and Dénes, Ádám},
	doi = {10.1084/jem.20211071},
	journal-iso = {J EXP MED},
	journal = {JOURNAL OF EXPERIMENTAL MEDICINE},
	volume = {219},
	unique-id = {32710992},
	issn = {0022-1007},
	abstract = {Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive. Here, we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. Microglia establish direct, dynamic purinergic contacts with cells in the neurovascular unit that shape CBF in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in mice, which is reiterated by chemogenetically induced microglial dysfunction associated with impaired ATP sensitivity. Hypercapnia induces rapid microglial calcium changes, P2Y12R-mediated formation of perivascular phylopodia, and microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Microglial actions modulate vascular cyclic GMP levels but are partially independent of nitric oxide. Finally, microglial dysfunction markedly impairs P2Y12R-mediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases.},
	year = {2022},
	eissn = {1540-9538},
	orcid-numbers = {Császár, Eszter/0000-0002-5543-4100; Lénárt, Nikolett/0000-0002-7456-949X; Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X; Szöllősi, Dávid/0000-0002-3363-3862; Tóthné Sviatkó, Katalin/0000-0002-5104-0884; Hricisák, László/0000-0001-8320-2166; Benyó, Zoltán/0000-0001-6015-0359; Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:33111942,
	title = {Microglial control of neuronal development via somatic purinergic junctions},
	url = {https://m2.mtmt.hu/api/publication/33111942},
	author = {Cserép, Csaba and Schwarcz, Dóra Anett and Pósfai, Balázs and László, Zsófia Ilona and Kellermayer, Anna and Környei, Zsuzsanna and Kisfali, Máté and Nyerges, Miklós and Lele, Zsolt and Katona, István and Dénes, Ádám},
	doi = {10.1016/j.celrep.2022.111369},
	journal-iso = {CELL REP},
	journal = {CELL REPORTS},
	volume = {40},
	unique-id = {33111942},
	issn = {2639-1856},
	year = {2022},
	eissn = {2211-1247},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X}
}

@article{MTMT:31790751,
	title = {Shaping Neuronal Fate: Functional Heterogeneity of Direct Microglia-Neuron Interactions},
	url = {https://m2.mtmt.hu/api/publication/31790751},
	author = {Cserép, Csaba and Pósfai, Balázs and Dénes, Ádám},
	doi = {10.1016/j.neuron.2020.11.007},
	journal-iso = {NEURON},
	journal = {NEURON},
	volume = {109},
	unique-id = {31790751},
	issn = {0896-6273},
	abstract = {The functional contribution of microglia to normal brain development, healthy brain function, and neurological disorders is increasingly recognized. However, until recently, the nature of intercellular interactions mediating these effects remained largely unclear. Recent findings show microglia establishing direct contact with different compartments of neurons. Although communication between microglia and neurons involves intermediate cells and soluble factors, direct membrane contacts enable a more precisely regulated, dynamic, and highly effective form of interaction for fine-tuning neuronal responses and fate. Here, we summarize the known ultrastructural, molecular, and functional features of direct microglia-neuron interactions and their roles in brain disease. © 2020 Elsevier Inc. In this review, Cserép et al. summarize the compartment-specific ultrastructural, molecular, and functional features of direct microglia-neuron interactions and their role in disease. © 2020 Elsevier Inc.},
	keywords = {▪▪▪},
	year = {2021},
	eissn = {1097-4199},
	pages = {222-240},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Pósfai, Balázs/0000-0003-1035-565X}
}