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1.

001-es BibID:BIBFORM103087
035-os BibID:(cikkazonosító)183108 (WOS)000207688800001 (Scopus)62749135020
Első szerző:Kiss-Tóth Éva (biológus)
Cím:PPAR gamma in kidney physiology and pathophysiology / Éva Kiss-Tóth, Tamás Röszer
Dátum:2008
ISSN:1687-4757 1687-4765
Megjegyzések:Involvement of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) in kidney physiology has been explored recently. Synthetic PPAR gamma ligands can ameliorate the diabetic kidney disease through different mechanisms, involving inhibition of mesangial cell growth, reduction of mesangial matrix, and cytokine production of glomerular cells as well as promoting endothelial cell survival within the kidney glomeruli. Activation of PPAR gamma has additional profibrotic consequences, which can contribute to wound healing in diabetic glomerulonephritis. Beside many beneficial effects, PPAR gamma activation, however, can lead to severe water retention, a common side effect of thiazolidinedione therapy. This unwanted effect is due to the activation of PPAR gamma in the mesonephric distal collecting system, where PPAR gamma positively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Recent studies indicate that PPAR gamma is also involved in the normal kidney development, renal lipid metabolism, and activation of the renin-angiotensin system. In this paper, we give a synopsis of the current knowledge on PPAR gamma functions in kidney phyisology and pathophysiology.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:PPAR Research. - 2008 (2008), p. 1-9. -
További szerzők:Röszer Tamás (1979-) (orvos, biológus)
Pályázati támogatás:OTKA-76091
OTKA
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2.

001-es BibID:BIBFORM103876
035-os BibID:(WoS)000253610100154
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Insulin resistance and enhanced ossification in mice with macrophage specific peroxisome proliferator activated receptor gamma deletion / Roszer T., Kiss-Toth E., Balogh L., Andocs G., Pintye E., Szanto A., Nagy L.
Dátum:2008
ISSN:0014-2972
Megjegyzések:Haploinsufficiency of nuclear receptor PPARcleads to enhanced osteoblast differentiation in mice. Althoughit is suggested, that PPARcof macrophages is involved in thepathomechanisms, their exact role is unknown
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:European Journal Of Clinical Investigation. - 38 : s1 (2008), p. 57. -
További szerzők:Kiss-Tóth Éva (1983-) (biológus) Balogh Lajos Andocs G. Pintye Éva (1955-) (fizikus) Szántó Attila (1976-) (orvos, biokémikus) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
Internet cím:Szerző által megadott URL
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM103137
035-os BibID:(WOS)000344348500008 (Scopus)84919882801
Első szerző:Röszer Tamás (orvos, biológus)
Cím:FMRF-amide is a glucose-lowering hormone in the snail Helix aspersa / Tamás Rőszer, Éva D. Kiss-Tóth
Dátum:2014
ISSN:0302-766X
Megjegyzések:Although glucose is metabolically the most important carbohydrate in almost all living organisms, still little is known about the evolution of the hormonal control of cellular glucose uptake. In this study, we identify Phe-Met-Arg-Phe-amide (FMRFa), also known as molluscan cardioexcitatory tetrapeptide, as a glucose-lowering hormone in the snail Helix aspersa. FMRFa belongs to an evolutionarily conserved neuropeptide family and is involved in the neuron-to-muscle signal transmission in the snail digestive system. This study shows that, beyond this function, FMRFa also has glucose-lowering activity. We found neuronal transcription of genes encoding FMRFa and its receptor and moreover the hemolymph FMRFa levels were peaking at metabolically active periods of the snails. In turn, hypometabolism of the dormant periods was associated with abolished FMRFa production. In the absence of FMRFa, the midintestinal gland ("hepatopancreas") cells were deficient in their glucose uptake, contributing to the development of glucose intolerance. Exogenous FMRFa restored the absorption of hemolymph glucose by the midintestinal gland cells and improved glucose tolerance in dormant snails. We show that FMRFa was released to the hemolymph in response to glucose challenge. FMRFa-containing nerve terminals reach the interstitial sinusoids between the chondroid cells in the artery walls. We propose that, in addition to the known sites of possible FMRFa secretion, these perivascular sinusoids serve as neurohemal organs and allow FMRFa release. This study suggests that in evolution, not only the insulin-like peptides have adopted the ability to increase cellular glucose uptake and can act as hypoglycemic hormones.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Glucose
Neuropeptide
Metabolism
Invertebrates
Hepatopancreas
Megjelenés:Cell And Tissue Research. - 358 : 2 (2014), p. 371-383. -
További szerzők:Kiss-Tóth Éva (1983-) (biológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM103106
035-os BibID:(WOS)000228340800003 (Scopus)19544370693
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Seasonal periodicity of enteric nitric oxide synthesis and its regulation in the snail, Helix lucorum / Tamás Röszer, Éva Kiss-Tóth, A. József Szentmiklósi, Gáspár Bánfalvi
Dátum:2005
ISSN:1077-8306
Megjegyzések:The snail Helix lucorum has been used as a model to study the adaptation of a nitric oxide (NO)-forming enteric neural network to the long-term resting period of summer estivation or winter hibernation. Quantification of the NO-derived nitrite established that NO formation is confined to the nitric oxide synthase (NOS)-containing myenteric network of the mid-intestine. In active snails but not in resting snails, NO production could be enhanced by the NOS substrate l-arginine (l-ARG, 1?mM). We followed the enteric NO synthesis in a snail population kept at natural conditions for 1 year. Our findings indicate that NO synthesis was depressed in July during entry to the estivation, had a peak in autumn before hibernation, and finally was reduced during hibernation. Monoamines (histamine, serotonin, and adrenalin) could inhibit the NO liberation in active snails. Cofactors of NOS (?-NADPH, ?-NAD, FAD, FMN, Ca2+, TH4) did not alter the low nitrite production in hibernating snails. We conclude that enteric NO synthesis in H. lucorum has a regular seasonal periodicity following the annual physiological cycles of terrestrial snails. During estivation or hibernation, NOS activity is blocked. Monoamines, the levels of which are elevated during hibernation, can trigger decreased NOS activity. The reduced activity of NOS cannot be restored by the administration of NOS cofactors; therefore, their absence cannot be the cause of the temporarily blocked L-ARG/NO conversion ability of NOS.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
NADPH diaphorase
nitric oxide synthase
enteric nervous system
Helix lucorum
Megjelenés:Invertebrate Biology. - 124 : 1 (2005), p. 18-24. -
További szerzők:Kiss-Tóth Éva (1983-) (biológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész)
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM065063
035-os BibID:(Wos)000334175100018 (Scopus)84898634971
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Leptin receptor deficient diabetic (db/db) mice are compromised in postnatal bone regeneration / Tamás Rőszer, Tamás Józsa, Éva D. Kiss-Tóth, Nora De Clerck, Lajos Balogh
Dátum:2014
ISSN:0302-766X
Megjegyzések:Increased fragility fracture risk with improper healing is a frequent and severe complication of insulin resistance (IR). The mechanisms impairing bone health in IR are still not fully appreciated, which gives importance to studies on bone pathologies in animal models of diabetes. Mice deficient in leptin signaling are widely used models of IR and its comorbidities. Leptin was first recognized as a hormone, regulating appetite and energy balance; however, recent studies have expanded its role showing that leptin is a link between insulin-dependent metabolism and bone homeostasis. In the light of these findings, it is intriguing to consider the role of leptin resistance in bone regeneration. In this study, we show that obese diabetic mice lacking leptin receptor (db/db) are deficient in postnatal regenerative osteogenesis. We apply an ectopic osteogenesis and a fracture healing model, both showing that db/db mice display compromised bone acquisition and regeneration capacity. The underlying mechanisms include delayed periosteal mesenchymatic osteogenesis, premature apoptosis of the cartilage callus and impaired microvascular invasion of the healing tissue. Our study supports the use of the db/db mouse as a model of IR associated bone-healing deficits and can aid further studies of mesenchymatic cell homing and differentiation, microvascular invasion, cartilage to bone transition and callus remodeling in diabetic fracture healing.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Fracture
Diabetes
Insulin resistance
LeptinBone
Megjelenés:Cell And Tissue Research. - 356 : 1 (2014), p. 195-206. -
További szerzők:Józsa Tamás (1969-) (gyermeksebész, urológus) Kiss-Tóth Éva (1983-) (biológus) De Clerk, Nora Balogh Lajos
Pályázati támogatás:OTKA 76091
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM012888
035-os BibID:(Wos)000284665200006 (Scopus)78649333360
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Hypothermia translocates nitric oxide synthase from cytosol to membrane in snail neurons / Tamás Rőszer, Éva Kiss-Tóth, Dávid Rózsa, Tamás Józsa, A. József Szentmiklósi, Gáspár Bánfalvi
Dátum:2010
Megjegyzések:Neuronal nitric oxide (NO) levels are modulated through the control of catalytic activity of NO synthase (NOS). Although signals limiting excess NO synthesis are being extensively studied in the vertebrate nervous system, our knowledge is rather limited on the control of NOS in neurons of invertebrates. We have previously reported a transient inactivation of NOS in hibernating snails. In the present study, we aimed to understand the mechanism leading to blocked NO production during hypothermic periods of Helix pomatia. We have found that hypothermic challenge translocated NOS from the cytosol to the perinuclear endoplasmic reticulum, and that this cytosol to membrane trafficking was essential for inhibition of NO synthesis. Cold stress also downregulated NOS mRNA levels in snail neurons, although the amount of NOS protein remained unaffected in response to hypothermia. Our studies with cultured neurons and glia cells revealed that glia-neuron signaling may inhibit membrane binding and inactivation of NOS. We provide evidence that hypothermia keeps NO synthesis "hibernated" through subcellular redistribution of NOS.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
nitric oxide synthase
Megjelenés:Cell and Tissue Research. - 342 : 2 (2010), p. 191-203. -
További szerzők:Kiss-Tóth Éva (1983-) (biológus) Rózsa Dávid (1982-) (Ph.D hallgató) Józsa Tamás (1969-) (gyermeksebész, urológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM001263
035-os BibID:(Wos)000239248000017 (Scopus)33746435763
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Phe-met-arg-phe (FMRF)-amide is a substrate source of NO synthase in the gastropod nervous system / Tamás Rőszer, Éva Kiss-Tóth, Mihály Petkó, A. József Szentmiklósi, Gáspár Bánfalvi
Dátum:2006
Megjegyzések:The possible involvement of the L-arginine-containing Phe-met-arg-phe (FMRF)-amide (FMRFa) in neuronal nitric oxide (NO) biosynthesis was studied in a gastropod species. We found NADPH-diaphorase-positive neurons and FMRFa-containing fibers in close proximity in the enteric nervous system. Administration of L-arginine and FMRFa induced quantitatively similar nitrite production in both intact intestinal tissues and tissue homogenates. These changes could be prevented by the presence of NOARG (an NO synthase inhibitor). Neither chemically modified FMRFa (D-arginine instead of L-arginine) nor amino acid constituents of FMRFa (methionine, phenylalanine) affected basal nitrite production. FMRFa-induced alterations were reduced in the presence of Na+ channel blockers (tetrodotoxin, amiloride, lidocaine), the Na+/K+ATPase inhibitor ouabain, or protease inhibitors (leupeptine, pepstatine-a). FMRFa and its amino acid constituents were analyzed by paper chromatography. When FMRFa was added to tissue homogenates, the peptide was eliminated within 1-2 min, whereas methionine, phenylalanine, arginine, and citrulline levels were elevated simultaneously. We tested the effects of FMRFa, L-arginine, and NOARG on intestinal contractile activity. FMRFa relaxed the intestine for 1-2 min and then induced contractions for 20-40 min. In the presence of NOARG, no relaxant effect of FMRFa was recorded. As administration of L-arginine strongly inhibits the mechanical activity of the intestinal muscle, NO production presumably plays a substantial role in the action of FMRFa, at least in the initial phase. Our biochemical data indicate a direct involvement of FMRFa in NO biosynthesis. FMRFa might be hydrolyzed by extracellular peptidases and then the locally released arginine might be transported into the cells and broken-down to produce NO. Depolarization-induced NO production attributable to the activation of amiloride-sensitive Na+ channels might also be involved.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
neuropeptid NO szintáz szubsztrát
Megjelenés:Cell and Tissue Research. - 325 : 3 (2006), p. 567-575. -
További szerzők:Kiss-Tóth Éva (1983-) (biológus) Petkó Mihály (1943-) (orvos, neurobiológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész)
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