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001-es BibID:	BIBFORM109585
035-os BibID:	(Scopus)85150718609 (WoS)000951373400001
Első szerző:	Ducza László (molekuláris biológus)
Cím:	Neuronal P2X4 receptor may contribute to peripheral inflammatory pain in rat spinal dorsal horn / Ducza László, Gajtkó Andrea, Hegedűs Krisztina, Bakk Erzsébet, Kis Gréta, Gaál Botond, Takács Roland, Szücs Péter, Matesz Klára, Holló Krisztina
Dátum:	2023
ISSN:	1662-5099
Megjegyzések:	Objective: Intense inflammation may result in pain, which manifests as spinal central sensitization. There is growing evidence that purinergic signaling plays a pivotal role in the orchestration of pain processing. Over the last decade the ionotropic P2X purino receptor 4 (P2X4) got into spotlight in neuropathic disorders, however its precise spinal expression was scantily characterized during inflammatory pain. Thus, we intended to analyze the receptor distribution within spinal dorsal horn and lumbar dorsal root ganglia (DRG) of rats suffering in inflammatory pain induced by complete Freund adjuvant (CFA). Methods: CFA-induced peripheral inflammation was validated by mechanical and thermal behavioral tests. In order to ensure about the putative alteration of spinal P2X4 receptor gene expression qPCR reactions were designed, followed by immunoperoxidase and Western blot experiments to assess changes at a protein level. Colocalization of P2X4 with neuronal and glial markers was investigated by double immunofluorescent labelings, which were subsequently analyzed with IMARIS software. Transmission electronmicroscopy was applied to study the ultrastructural localization of the receptor. Concurrently, in lumbar DRG cells similar methodology has been carried out to complete our observations. Results: The figures of mechanical and thermal behavioral tests proved the establishment of CFA-induced inflammatory pain. We observed significant enhancement of P2X4 transcript level within the spinal dorsal horn 3?days upon CFA administration. Elevation of P2X4 immunoreactivity within Rexed lamina I-II of the spinal gray matter was synchronous with mRNA expression, and confirmed by protein blotting. According to IMARIS analysis the robust protein increase was mainly detected on primary afferent axonterminals and GFAP-labelled astrocyte membrane compartments, but not on postsynaptic dendrites was also validated ultrastructurally within the spinal dorsal horn. Furthermore, lumbar DRG analysis demonstrated that peptidergic and non-peptidergic nociceptive subsets of ganglia cells were also abundantly positive for P2X4 receptor in CFA model. Conclusion: Here we provide novel evidence about involvement of neuronal and glial P2X4 receptor in the establishment of inflammatory pain.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk inflammatory pain spinal dorsal horn P2X4 receptor central sensitization primary afferents glial cells dorsal root ganglia
Megjelenés:	Frontiers in Molecular Neuroscience. - 16 (2023), p. 1-16. -
További szerzők:	Gajtkó Andrea (1989-) (molekuláris biológus) Hegedűs Krisztina Bakk Erzsébet Kis Gréta (1979-) (molekuláris biológus) Gaál Botond Ágoston (1982-) (anatómus, neurobiológus) Takács Roland Ádám (1985-) (molekuláris biológus, biokémikus) Szűcs Péter (1974-) (kutatóorvos) Matesz Klára (1949-) (anatómus, neurobiológus) Holló Krisztina (1967-) (vegyész)
Pályázati támogatás:	KTIA_NAP_13-2-2014-0005 Egyéb 2017-1.2.1-NKP-2017-00002 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM131018
035-os BibID:	(wos)001520635500001
Első szerző:	Gaál Botond Ágoston (anatómus, neurobiológus)
Cím:	The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain : molecular Mechanisms and Therapeutic Opportunities / Gaál Botond, Takács Roland, Matta Csaba, Juhász Krisztián, Fülesdi Béla, Szekanecz Zoltán, Benkő Szilvia, Ducza László
Dátum:	2025
ISSN:	2152-5250
Megjegyzések:	Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, synaptic dysfunction, and chronic neuroinflammation. Mounting evidence suggests that inflammasome activation plays a pivotal role in the onset and progression of AD by promoting neuronal damage, Tau pathology, and amyloid-? (A?) accumulation. Among the various inflammasome types expressed in the central nervous system (CNS), NLRP3 has received particular attention due to its strong association with both AD and pain-related neuroinflammation. Chronic pain, frequently observed in older adults and individuals with dementia, shares overlapping inflammatory mechanisms with AD, including glial activation and cytokine dysregulation. The inflammasome-microRNA (miR) axis has recently emerged as a key regulatory pathway modulating these neuroinflammatory responses. Specific inflammation-associated miRs, such as miR-22, miR-34a, miR-146a, miR-155, and miR-223, influence innate immune signaling and critically affect both neuronal homeostasis and pain sensitization. Emerging evidence also implicates dysfunction of the locus coeruleus-noradrenergic (LC-NE) system?an early target of AD pathology?in amplifying neuroinflammation and pain sensitivity, partly through interactions with dysregulated miRs. While previous studies have addressed the roles of inflamma-miRs in AD or chronic pain individually, this review uniquely examines their interconnected roles?highlighting how dysregulated miR expression and inflammasome activation may converge to drive persistent neuroinflammation across both conditions. By elucidating shared molecular pathways, we propose that targeting the inflammasome-miR axis may offer dual therapeutic potential: slowing AD progression while addressing pain-related neural dysfunction. As the prevalence of AD rises, such integrated insights are essential for the development of more precise, mechanism-based interventions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Alzheimer's disease Chronic pain Neuroinflammation Inflammasome MicroRNA Spinal cord Glia
Megjelenés:	Aging and Disease. - [Epub ahead of print] (2025). -
További szerzők:	Takács Roland Ádám (1985-) (molekuláris biológus, biokémikus) Matta Csaba (1980-) (molekuláris biológus, genetikus, angol szakfordító) Juhász Krisztián Zoltán (1998-) (molekuláris biológus) Fülesdi Béla (1961-) (aneszteziológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Benkő Szilvia (1973-) (molekuláris biológus) Ducza László (1987-) (molekuláris biológus)
Pályázati támogatás:	FK-134304 OTKA EKÖP-24-4-II-DE-58 Egyéb EKÖP-24-3-I-DE-29 Egyéb K131844 OTKA BO/125/13 MTA K147109 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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