CCL

Összesen 9 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM103109
035-os BibID:(Wos)000369324800011 (Scopus)84956924801
Első szerző:Ampem, Grace
Cím:Adipose tissue macrophages in non-rodent mammals : a comparative study / Grace Ampem, Hind Azegrouz, Árpád Bacsadi, Lajos Balogh, Susanne Schmidt, Julianna Thuróczy, Tamás Röszer
Dátum:2015
ISSN:0302-766X
Megjegyzések:The stromal vascular fraction (SVF) of adipose tissue in rodents and primates contains mesenchymal stem cells and immune cells. SVF cells have complex metabolic, immune and endocrine functions with biomedical impact. However, in other mammals, the amount of data on SVF stem cells is negligible and whether the SVF hosts immune cells is unknown. In this study, we show that the SVF is rich in immune cells, with a dominance of adipose tissue macrophages (ATMs) in cattle (Bos primigenius taurus), domestic goat (Capra aegagrus hircus), domestic sheep (Ovis aries), domestic cat (Felis catus) and domestic dog (Canis familiaris). ATMs of these species are granulated lysosome-rich cells with lamellipodial protrusions and express the lysosome markers acid phosphatase 5 (ACP-5) and Mac-3/Lamp-2. Using ACP-5 and Mac-3/Lamp-2 as markers, we additionally detected ATMs in other species, such as the domestic horse (Equus ferus caballus), wild boar (Sus scrofa) and red fox (Vulpes vulpes). Feline and canine ATMs also express the murine macrophage marker F4/80 antigen. In the lean condition, the alternative macrophage activation marker CD206 is expressed by feline and canine ATMs and arginase-1 by feline ATMs. Obesity is associated with interleukin-6 and interferon gamma expression and with overt tyrosine nitration in both feline and canine ATMs. This resembles the obesity-induced phenotype switch of murine and human ATMs. Thus, we show, for the first time, that the presence of ATMs is a general trait of mammals. The interaction between the adipose cells and SVF immune cells might be evolutionarily conserved among mammals.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Macrophages
Adipose tissue
Inflammation
Alternative activation
Metabolism
Mammals
Megjelenés:Cell And Tissue Research. - 363 : 2 (2015), p. 461-478. -
További szerzők:Azegrouz, Hind Bacsadi Árpád Balogh Lajos Schmidt, Susanne Thuróczy Julianna Röszer Tamás (1979-) (orvos, biológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM103092
035-os BibID:(Wos)000487075100007 (Scopus)85064700512
Első szerző:Ampem, Grace
Cím:The environmental obesogen bisphenol A increases macrophage self-renewal / Grace Ampem, Alexandra Junginger, Haidong Yu, Lajos Balogh, Julianna Thuróczy, Marion E. Schneider, Tamás Röszer
Dátum:2019
ISSN:0302-766X
Megjegyzések:Self-renewal of macrophages is important for the healthy development and replenishment of tissue-resident macrophage pools. How this mechanism is controlled by endocrine signals is still largely unexplored. Here, we show that the endocrine disruptor bisphenol A (BPA) increases macrophage self-renewal. This effect was associated with phosphorylation of extracellular signal-regulated kinase (ERK) and a slight increase in the expression of liver X receptor alpha (LXRalpha). We found that LXRaplha inhibition induced, while LXRalpha activation impeded, macrophage self-renewal. LXRalpha signaling hence may protect from excessive macrophage expansion. Self-renewing macrophages, however, had negligible LXR expression when compared with quiescent macrophages. Accordingly, tissue-resident macrophage pools, which are dominated by quiescent macrophages, were rich in LXRalpha-expressing macrophages. Overall, we show that BPA increases macrophage self-renewal and that this effect, at least in part, can be inhibited by increasing LXRalpha expression. Since BPA is accumulated in the adipose tissue, it has the potential to increase self-renewal of adipose tissue macrophages, leading to a condition that might negatively impact adipose tissue health.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Endocrine disruptors
ERK
LXR
Obesity
Obesogens
Megjelenés:Cell And Tissue Research. - 378 : 1 (2019), p. 81-96. -
További szerzők:Junginger, Alexandra Yu, Haidong Balogh Lajos Thuróczy Julianna Schneider, Marion E. Röszer Tamás (1979-) (orvos, biológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM103146
035-os BibID:(Wos)000345083700004 (Scopus)84919799226
Első szerző:Röszer Tamás (orvos, biológus)
Cím:The invertebrate midintestinal gland ("hepatopancreas") is an evolutionary forerunner in the integration of immunity and metabolism / Tamás Röszer
Dátum:2014
ISSN:0302-766X
Megjegyzések:The immune system has an impact on the metabolic performance in vertebrates, thus the metabolic effects of immune cells are receiving intense attention today in the biomedical field. However, the evolutionary origin of the immunity-metabolism interaction is still uncertain. In this review, I show that mollusks and crustaceans integrate immune functions to a metabolic organ, the midintestinal gland ("hepatopancreas"). In these animals, the epithelial cells of the midintestinal gland are major sources of immune molecules, such as lectins, hemocyanin, ferritin, antibacterial and antiviral proteins, proteolytic enzymes and nitric oxide. There is crosstalk between midintestinal gland cells and phagocytes, which aids the initiation of the immune response and the clearance of pathogens. The midintestinal gland is thereby an integrated organ of immunity and metabolism. It is likely that immunity was the primary function of the midintestinal gland cells and that their role in the intermediate metabolism has evolved during the course of their further specialization.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Evolution
Hepatopancreas
Immunity
Invertebrates
Metabolism
Megjelenés:Cell And Tissue Research. - 358 : 3 (2014), p. 685-695. -
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

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
Borító:

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
Borító:

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
Borító:

7.

001-es BibID:BIBFORM008293
035-os BibID:(Wos)000265622700014 (Scopus)67349249432
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Acetylcholine inhibits nitric oxide (NO) synthesis in the gastropod nervous system / Tamás Rőszer, Tamás Józsa, A. József Szentmiklósi, Gáspár Bánfalvi
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Cell and Tissue Research. - 336 : 2 (2009), p. 325-335. -
További szerzők:Józsa Tamás (1969-) (gyermeksebész, urológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész)
Internet cím:elektronikus változat
DOI
Borító:

8.

001-es BibID:BIBFORM003340
035-os BibID:(Wos)000220863100011 (Scopus)2442660388
Első szerző:Röszer Tamás (orvos, biológus)
Cím:Nitric oxide synthesis is blocked in the enteral nervous system during dormant periods of the snail Helix lucorum L. / Tamás Rőszer, Zsolt Czimmerer, A. József Szentmiklósi, Gáspár Bánfalvi
Dátum:2004
ISSN:0302-766X
Megjegyzések:During dormancy of terrestrial snails, the whole neuromodulation of the nervous system is deeply modified. In this work we studied the adaptation of a previously described, putatively nitric oxide (NO) forming enteral network to the long-term resting periods of the snail Helix lucorum. The standard NADPH diaphorase (NADPHd) technique, which is an accepted method for histochemical NO synthase (NOS) detection, labeled the same enteric neurons of the midintestine in active or hibernated snails. Quantification of the NO-derived nitrite by the Griess reaction established that the nitrite formation is confined to the NADPHd-reactive network containing the midintestinal segment. In active snails, the nitrite formation could be enhanced by the NOS substrate l-arginine (10 mM?1 mM), but decreased by the known NOS inhibitors 1 mM Nw-nitro-l-arginine (NOARG) and 10 mM aminoguanidine (AG). Application of 1 mM larginine and 1 mM NOARG decreased the amplitude of the midintestinal muscle contractile activity, but did not affect the rectal motility. In dormancy, the nitrite formation was reduced in the NADPHd-reactive midintestinal network. Application of l-arginine could not provoke nitrite production and did not influence the midintestinal motility. Our findings indicate that NO is involved in the neural transmission to intestinal muscles of gastropods, but enteric release of NO is blocked during dormancy. The decreased NO synthesis is possibly due to an as yet undefined mechanism, by which the l-arginine/NO conversion ability of NOS could temporarily be inhibited in the long-term resting period of H. lucorum.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
NADPH diaphorase
nitric oxide synthase
hibernation
estivation
enteric nervous system
Helix lucorum L. (Mollusca)
Megjelenés:Cell and tissue research. - 316 (2004), p. 255-262. -
További szerzők:Czimmerer Zsolt (1981-) (molekuláris biológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bánfalvi Gáspár (1943-) (sejtbiológus, gyógyszerész)
Internet cím:elektronikus változat
Borító:

9.

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)
Internet cím:elektronikus változat
DOI
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.