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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:	BIBFORM015066
035-os BibID:	(WOS)000297855700007 (Scopus)82455174750
Első szerző:	Galajda Zoltán (szívsebész, érsebész)
Cím:	Histamine and H1-Histamine receptors faster venous circulation / Zoltan Galajda, Jozsef Balla, A. Jozsef Szentmiklosi, Tamas Biro, Gabriella Czifra, Nora Dobrosi, Agnes Cseppento, Lajos Patonay, Tamas Roszer, Gyorgy Balla, Laurenciu M. Popescu, Istvan Lekli, Arpad Tosaki
Dátum:	2011
Megjegyzések:	The study has analysed the action of histamine in the rabbit venous system and evaluated its potential role in contraction during increased venous pressure. We have found that a great variety exists in histamine sensitivity and H1-histamine receptor expression in various types of rabbit veins. Veins of the extremities (saphenous vein, femoral vein, axillary vein) and abdomen (common iliac vein, inferior vena cava) responded to histamine by a prominent, concentration-dependent force generation, whereas great thoracic veins (subclavian vein, superior vena cavas, intrathoracic part of inferior vena cava) and a pelvic vein (external iliac vein) exhibited slight sensitivity to exogenous histamine. The lack of reactivity to histamine was not due to increased activity of nitric oxide synthase (NOS) or heme oxygenase-1. H1-histamine receptor expression of veins correlated well with the histamine-induced contractions. Voltage-dependent calcium channels mediated mainly the histamine-induced force generation of saphenous vein, whereas it did not act in the inferior vena cava. In contrast, the receptor-operated channels were not involved in this response in either vein. Tyrosine phosphorylation occurred markedly in response to histamine in the saphenous vein, but not in the inferior vena cava. Histamine induced a prominent p kinase activation in both vessels. Protein kinase C and mitogen-activated protein kinase (MAPK) were not implicated in the histamine-induced intracellular calcium sensitization. Importantly, transient clamping of the femoral vein in animals caused a short-term constriction, which was inhibited by H1-histamine receptor antagonist in vivo. Furthermore, a significantly greater histamine immunopositivity was detected in veins after stretching compared to the resting state. We conclude that histamine receptor density adapts to the actual requirements of the circulation, and histamine liberated by the venous wall during increased venous pressure contributes to the contraction of vessels, providing a force for the venous return.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Molekuláris Medicina
Megjelenés:	Journal of Cellular and Molecular Medicine. - 15 : 12 (2011), p. 2614-2623. -
További szerzők:	Balla József (1959-) (belgyógyász, nephrológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bíró Tamás (1968-) (élettanász) Czifra Gabriella (1975-) (élettanász) Dobrosi Nóra (1981-) (molekuláris biológus) Cseppentő Ágnes (1953-) (orvos) Patonay Lajos (anatómus) Röszer Tamás (1979-) (orvos, biológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Popescu, Laurenciu M. Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Vaszkuláris biológia K-72315 OTKA TÁMOP 4.2.2-08/1-2008-0007 TÁMOP ETT 586/2006 EGYÉB ETT 147/2009 EGYÉB K 75883 OTKA K 83478 OTKA MTA-DE-11003 EGYÉB
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM060757
Első szerző:	Szabó Tamás (gyermekgyógyász)
Cím:	Regulation of TRPC6 ion channels in podocytes : implications for focal segmental glomerulosclerosis and acquired forms of proteinuric diseases / T. Szabó, L. Ambrus, N. Zákány, Gy. Balla, T. Bíró
Dátum:	2015
ISSN:	0231-424X 1588-2683
Megjegyzések:	The glomerular filtration barrier is a highly specialized tri-layer structure with unique functional properties. Podocyte dysfunction and cytoskeletal disorganization leads to disruption of the slit diaphragma, and proteinuria. Inflammatory diseases involving the kidney as well as inherited podocytopathies or diabetic nephropathy cause injury of the podocyte network. Focal segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common cause of nephrotic syndrome with severe proteinuria in both adults and children. Several causative genes have been identified in the pathogenesis of FSGS. Mutations of the transient receptor potential canonical-6 (TRPC6), a non-selective cation channel that is directly activated by diacylglycerol (DAG), cause a particularly aggressive form of FSGS. Angiotensin II, acting through its AT1 receptor, plays a critical role in generation of proteinuria and progression of kidney injury in a number of kidney diseases, including FSGS. Mounting evidence suggest the central role of TRPC6 and perhaps other TRPC channels in the pathogenesis of FSGS as well as of acquired forms of proteinuria such as diabetic nephropathy or hypertension. Identification of signaling pathways downstream of TRPC6 may provide novel targets for the treatment of proteinuria and prevent progression of podocyte injury.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény hazai lapban proteinuric disease focal segmental glomerulosclerosis (FSGS) TRPC6 diabetic nephropathy angiotensin II podocyte
Megjelenés:	Acta Physiologica Hungarica 102 : 3 (2015), p. 241-251. -
További szerzők:	Ambrus Lídia (1986-) (élettanász) Zákány Nóra Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Bíró Tamás (1968-) (élettanász)
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0045 TÁMOP Gyermekgyógyászat Kutatócsoport PD-76065 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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