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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)
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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)
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

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)
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

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
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5.

001-es BibID:BIBFORM103512
035-os BibID:(Wos)000408842300035 (Scopus)85055814380 (Pubmed)28758905
Első szerző:Waqas, Syed F. Hassnain
Cím:Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages(vol 127, pg 2842, 2017) / Syed F. Hassnain Waqas, Anh Cuong Hoang, Ya-Tin Lin, Grace Ampem, Hind Azegrouz, Lajos Balogh, Julianna Thuróczy, Jin-Chung Chen, Ivan C. Gerling, Sorim Nam, Jong-Seok Lim, Juncal Martinez-Ibañez, José T. Real, Stephan Paschke, Raphaëlle Quillet, Safia Ayachi, Frédéric Simonin, E. Marion Schneider, Jacqueline A. Brinkman, Dudley W. Lamming, Christine M. Seroogy, Tamás Röszer
Dátum:2017
ISSN:0021-9738
Tárgyszavak:Orvostudományok Elméleti orvostudományok hozzászólás
folyóiratcikk
Megjelenés:Journal of Clinical Investigation. - 127 : 9 (2017), p. 3559. -
További szerzők:Hoang, Anh Cuong Lin, Ya-Tin Ampem, Grace Azegrouz, Hind Balogh Lajos Thuróczy Julianna Chen, Jin-Chung Gerling, Ivan C. Nam, Sorim Lim, Jong-Seok Martinez-Ibanez, Juncal Real, José T. Paschke, Stephan Quillet, Raphaëlle Ayachi, Safia Simonin, Frédéric Schneider, Marion E. Brinkman, Jacqueline A. Lamming, Dudley W. Seroogy, Christine M. Röszer Tamás (1979-) (orvos, biológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM103105
035-os BibID:(Wos)000404557400039 (Scopus)85021739476
Első szerző:Waqas, Syed F. Hassnain
Cím:Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages / Syed F. Hassnain Waqas, Anh Cuong Hoang, Ya-Tin Lin, Grace Ampem, Hind Azegrouz, Lajos Balogh, Julianna Thuróczy, Jin-Chung Chen, Ivan C. Gerling, Sorim Nam, Jong-Seok Lim, Juncal Martinez-Ibanez, José T. Real, Stephan Paschke, Raphaëlle Quillet, Safia Ayachi, Frédéric Simonin, E. Marion Schneider, Jacqueline A. Brinkman, Dudley W. Lamming, Christine M. Seroogy, Tamás Röszer
Dátum:2017
ISSN:0021-9738
Megjegyzések:The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM proliferation were abolished in NPFFR2-deficient ATMs. Mechanistically, the effects of NPFF involved the suppression of E3 ubiquitin ligase RNF128 expression, resulting in enhanced stability of phosphorylated STAT6 and increased transcription of the M2 macrophage-associated genes IL-4 receptor alpha (Il4ra), arginase 1 (Arg1), IL-10 (Il10), and alkylglycerol monooxygenase (Agmo). NPFF induced ATM proliferation concomitantly with the increase in N-Myc downstream-regulated gene 2 (Ndrg2) expression and suppressed the transcription of Ifi200 cell-cycle inhibitor family members and MAF bZIP transcription factor B (Mafb), a negative regulator of macrophage proliferation. NPFF thus plays an important role in supporting healthy adipose tissue via the maintenance of metabolically beneficial ATMs.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Clinical Investigation. - 127 : 7 (2017), p. 2842-2854. -
További szerzők:Hoang, Anh Cuong Lin, Ya-Tin Ampem, Grace Azegrouz, Hind Balogh Lajos Thuróczy Julianna Chen, Jin-Chung Gerling, Ivan C. Nam, Sorim Lim, Jong-Seok Martinez-Ibanez, Juncal Real, José T. Paschke, Stephan Quillet, Raphaëlle Ayachi, Safia Simonin, Frédéric Schneider, Marion E. Brinkman, Jacqueline A. Lamming, Dudley W. Seroogy, Christine M. Röszer Tamás (1979-) (orvos, biológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM103080
035-os BibID:(Wos)000470082800036 (Scopus)85066061092
Első szerző:Yu, Haidong
Cím:Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages / Haidong Yu, Sedat Dilbaz, Jonas Comann, Anh Cuong Hoang, Victoria Diedrich, Annika Herwig, Akiko Harauma, Yukino Hoshi, Toru Moriguchi, Kathrin Landgraf, Antje Körner, Christina Lucas, Susanne Brodesser, Lajos Balogh, Julianna Thuróczy, Gopal Karemore, Michael Scott Kuefner, Edwards A. Park, Christine Rapp, Jeffrey Bryant Travers, Tamás Röszer
Dátum:2019
ISSN:0021-9738
Megjegyzések:Prevalence of obesity among infants and children below 5 years of age is rising dramatically, and early childhood obesity is a forerunner of obesity and obesity-associated diseases in adulthood. Childhood obesity is hence one of the most serious public health challenges today. Here, we have identified a mother-to-child lipid signaling that protects from obesity. We have found that breast milk-specific lipid species, so-called alkylglycerol-type (AKG-type) ether lipids, which are absent from infant formula and adult-type diets, maintain beige adipose tissue (BeAT) in the infant and impede the transformation of BeAT into lipid-storing white adipose tissue (WAT). Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of AKG intake in infancy leads to a premature loss of BeAT and increases fat accumulation. AKG signaling is specific for infants and is inactivated in adulthood. However, in obese adipose tissue, ATMs regain their ability to metabolize AKGs, which reduces obesity. In summary, AKGs are specific lipid signals of breast milk that are essential for healthy adipose tissue development.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Adipose tissue
Immunology
Macrophages
Metabolism
Obesity
Megjelenés:Journal Of Clinical Investigation. - 129 : 6 (2019), p. 2485-2499. -
További szerzők:Dilbaz, Sedat Comann, Jonas Hoang, Anh Cuong Diedrich, Victoria Herwig, Annika Harauma, Akiko Hoshi, Yukino Moriguchi, Toru Landgraf, Kathrin Körner, Antje Lucas, Christina Brodesser, Susanne Balogh Lajos Thuróczy Julianna Karemore, Gopal Kuefner, Michael Scott Park, Edwards A. Rapp, Christine Travers, Jeffrey Bryant Röszer Tamás (1979-) (orvos, biológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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