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001-es BibID:	BIBFORM060756
Első szerző:	Ambrus Lídia (élettanász)
Cím:	Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes / Lídia Ambrus, Attila Oláh, Tamás Oláh, György Balla, Moin A. Saleem, Petronella Orosz, Judit Zsuga, Klára Bíró, László Csernoch, Tamás Bíró, Tamás Szabó
Dátum:	2015
ISSN:	1582-1838
Megjegyzések:	Transient receptor potential canonical-6 (TRPC6) ion channels, expressed at high levels in podocytes of the filtration barrier, are recently implicated in the pathogenesis of various forms of proteinuric kidney diseases. Indeed, inherited or acquired up-regulation of TRPC6 activities are suggested to play a role in podocytopathies. Yet, we possess limited information about the regulation of TRPC6 in human podocytes. Therefore, in this study, we aimed at defining how the protein kinase C (PKC) system, one of the key intracellular signalling pathways, regulates TRPC6 function and expression. On human differentiated podocytes, we identified the molecular expressions of both TRPC6 and several PKC isoforms. We also showed that TRPC6 channels are functional since the TRPC6 activator 1-oleoyl-2-acetyl-sn-glycerol (OAG) induced Ca2+-influx to the cells. By assessing the regulatory roles of the PKCs, we found that inhibitors of the endogenous activities of classical and novel PKC isoforms markedly augmented TRPC6 activities. In contrast, activation of the PKC system by phorbol 12-myristate 13-acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Importantly, PMA treatment markedly down-regulated the expression levels of PKCa, PKCb, and PKCg reflecting their activation. Taken together, these results indicate that the PKC system exhibits a 'tonic' inhibition on TRPC6 activity in human podocytes suggesting that pathological conditions altering the expression and/or activation patterns of podocyte-expressed PKCs may influence TRPC6 activity and hence podocyte functions. Therefore, it is proposed that targeted manipulation of certain PKC isoforms might be beneficial in certain proteinuric kidney diseases with altered TRPC6 functions.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban human podocytes transient receptor potential canonical-6 protein kinase C isoforms proteinuria
Megjelenés:	Journal Of Cellular And Molecular Medicine. - 19 : 12 (2015), p. 2771-2779. -
További szerzők:	Oláh Attila (1984-) (élettanász) Oláh Tamás (1983-) (élettanász) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Saleem, Moin A. Orosz Petronella (1986-) (klinikai orvos) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Bíró Klára (1970-) (egészségügyi menedzsment) Csernoch László (1961-) (élettanász) Bíró Tamás (1968-) (élettanász) Szabó Tamás (1968-) (gyermekgyógyász)
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP Gyermekgyógyászat Kutatócsoport
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM132555
035-os BibID:	(Scopus)105018652292 (WoS)001594666900001
Első szerző:	Singlár Zoltán (biotechnológus)
Cím:	Revealing the Specific Contributions of Mitochondrial CB1 Receptors to the Overall Function of Skeletal Muscle in Mice / Zoltán Singlár, Péter Szentesi, Nyamkhuu Ganbat, Barnabás Horváth, László Juhász, Mónika Gönczi, Anikó Keller-Pintér, Attila Oláh, Zoltán Máté, Ferenc Erdélyi, László Csernoch, Mónika Sztretye
Dátum:	2025
ISSN:	2073-4409
Megjegyzések:	Skeletal muscle, constituting 40?50% of total body mass, is vital for mobility, posture, and systemic homeostasis. Muscle contraction heavily relies on ATP, primarily generated by mitochondrial oxidative phosphorylation. Mitochondria play a key role in decoding intracellular calcium signals. The endocannabinoid system (ECS), including CB1 receptors (CB1Rs), broadly influences physiological processes and, in muscles, regulates functions like energy metabolism, development, and repair. While plasma membrane CB1Rs (pCB1Rs) are well-established, a distinct mitochondrial CB1R (mtCB1R) population also exists in muscles, influencing mitochondrial oxidative activity and quality control. We investigated the role of mtCB1Rs in skeletal muscle physiology using a novel systemic mitochondrial CB1 deletion murine model. Our in vivo studies showed no changes in motor function, coordination, or grip strength in mtCB1 knockout mice. However, in vitro force measurements revealed significantly reduced specific force in both fast-twitch (EDL) and slow-twitch (SOL) muscles following mtCB1R ablation. Interestingly, knockout EDL muscles exhibited hypertrophy, suggesting a compensatory response to reduced force quality. Electron microscopy revealed significant mitochondrial morphological abnormalities, including enlargement and irregular shapes, correlating with these functional deficits. High-resolution respirometry further demonstrated impaired mitochondrial respiration, with reduced oxidative phosphorylation and electron transport system capacities in knockout mitochondria. Crucially, mitochondrial membrane potential dissipated faster in mtCB1 knockout muscle fibers, whilst mitochondrial calcium levels were higher at rest. These findings collectively establish that mtCB1Rs are critical for maintaining mitochondrial health and function, directly impacting muscle energy production and contractile performance. Our results provide new insights into ECS-mediated regulation of skeletal muscle function and open therapeutic opportunities for muscle disorders and aging.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk ATP calcium homeostasis cannabinoid receptor type 1 mitochondria mitochondrial cannabinoid receptor type 1 murine skeletal muscle muscle force mtCB1 knockout skeletal endocannabinoid system
Megjelenés:	Cells. - 14 : 19 (2025), p. 1-26. -
További szerzők:	Szentesi Péter (1967-) (élettanász) Ganbat, Nyamkhuu (1995-) (molekuláris biológus) Horváth Barnabás Juhász László Gönczi Mónika (1974-) (élettanász) Keller-Pintér Anikó Oláh Attila (1984-) (élettanász) Máté Zoltán Erdélyi Ferenc Csernoch László (1961-) (élettanász) Sztretye Mónika (1981-) (élettanász, elektrofiziológus)
Pályázati támogatás:	NKFIH FK-142481 Egyéb NKFIH FK-134684 Egyéb NKFIH FK-134235 Egyéb NKFIH K-137600 Egyéb TKP2020-NKA-04 Egyéb TKP2021-EGA-28 Egyéb
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