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1.

001-es BibID:BIBFORM078592
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Role of heme in soft tissue mineralization / Balla József, Zarjou Abolfazl, Agarwal Anupam, Becs Gergely, Kovács Katalin, Nyitrai Mónika, Potor László, Pethő Dávid, Oros Melinda, Zavaczki Erzsébet, Arosio Paolo, Eaton John, Balla György
Dátum:2016
ISSN:0891-5849
Megjegyzések:Infiltration of red blood cells into atherosclerotic lesions is a common event in the progression of atherosclerosis. Recently we have observed that after infiltration and exposure of erythrocytes to plaque material, are lysed, and the liberated hemoglobin is oxidized to ferryl hemoglobin (FeIII/FeIV?O) and ferri (FeIII) hemoglobin. After oxidation of ferro (FeII) hemoglobin heme dissociates from globin then is translocated into resident cells including smooth muscle cells within arteries. Mounting evidence suggests an essential role for the heme oxygenase 1 (HO-1)/ferritin system to maintain homeostasis of vascular function. We examined whether induction of HO-1 and ferritin by heme alters mineralization of human smooth muscle cells provoked by phosphorous and vitamin D3 analogs. Upregulation of the HO-1/ferritin system inhibited human smooth muscle cells calcification and osteoblastic differentiation. Of the products of the system, only ferritin and, to a lesser extent, biliverdin were responsible for the inhibition. Ferritin heavy chain and ceruloplasmin, which both possess ferroxidase activity, inhibited calcification; a site-directed mutant of ferritin heavy chain, which lacked ferroxidase activity, failed to inhibit calcification. In addition, osteoblastic transformation of human smooth muscle cells (assessed by upregulation of core binding factor alpha-1, osteocalcin, and alkaline phosphatase activity) was diminished by ferritin/ferroxidase activity. Furthermore, iron-provoked inhibition of osteoblast activity was also demonstrated to be mediated by ferritin and its ferroxidase activity. We conclude that induction of the HO-1/ferritin system prevents calcification and osteoblastic differentiation of human smooth muscle cells mainly via the ferroxidase activity of ferritin.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
heme
mineralization
Megjelenés:Free Radical Biology And Medicine. - 96 (2016), p. S13. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Becs Gergely Sikura Katalin Éva (1985-) (biológus) Nyitrai Mónika Potor László Pethő Dávid Oros Melinda (1975-) (molekuláris biológus) Zavaczki Erzsébet (1983-) (biotechnológus) Arosio, Paolo Eaton, John W. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
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2.

001-es BibID:BIBFORM050620
Első szerző:Barta Kitti (belgyógyász)
Cím:Hemodiafiltration beneficially affects QT interval duration and dispersion compared to hemodialysis / Kitti Barta, Árpád Czifra, Csaba Kun, Alida Páll, Julianna Kulcsár, György Paragh, István Lőrincz, Tamás János Padra, Anupam Agarwal, Zarjou Abolfazl, József Balla, Zoltán Szabo
Dátum:2014
ISSN:1342-1751 1437-7799
Megjegyzések:BACKGROUND/AIMS:The prolongation of the QT interval and dispersion could predict ventricular arrhythmias. It is not yet established whether there is a difference between the effects of hemodialysis and hemodiafiltration on QT interval duration and dispersion.METHODS:Data of thirty patients was investigated while they were receiving hemodiafiltration over a period of 3 months; then the same group of patients was evaluated during treatment with conventional hemodialysis for at least another 3 months. Ionic parameters and surface electrocardiograms (ECG) were analyzed five times during each session, and 2D, M-mode echocardiography and Holter ECGs were performed to acquire additional information.RESULTS:QT interval duration (QTmax) and dispersion (QTd) showed a significant increase during hemodialysis, but not during hemodiafiltration. QTmax was 388.66 ? 31.81 ms at the beginning of hemodialysis and increased to 400.66 ? 39.12 ms even at the 30th minute (p < 0.05). QTd was found to be 31.33 ? 10.08 ms before the commencement of hemodialysis with the largest prolongation being seen at the 240th minute (51.33 ? 14.56 ms, p < 0.05). The occurrence of ventricular premature beats was significantly higher during hemodialysis (p = 0.018). The left atrial diameter significantly decreased at the end of hemodiafiltration (at the beginning 45.1 ? 5.25 mm, at the end 40.77 ? 5.76 mm; p < 0.05).CONCLUSION:Our results suggest a beneficial effect of hemodiafiltration on the studied electrocardiographic parameters compared to hemodialysis. The larger decrease in the left atrial diameter suggests a more efficient intracardiac volume-decreasing potential of hemodiafiltration.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Hemodiafiltration
Hemodialysis
Ventricular arrhythmias
QT interval
QT dispersion
Megjelenés:Clinical and Experimental Nephrology. - 18 : 6 (2014), p. 952-959. -
További szerzők:Czifra Árpád (1983-) (belgyógyász) Kun Csaba (1969-) (kardiológus) Páll Alida (1983-) (orvos) Kulcsár Júlia (1983-) (orvos) Paragh György (1953-) (belgyógyász) Lőrincz István (1950-) (belgyógyász, kardiológus) Padra János Tamás (1984-) (biológus) Agarwal, Anupam Zarjou, Abolfazl (1979-) (kutató orvos) Balla József (1959-) (belgyógyász, nephrológus) Szabó Zoltán (1973-) (belgyógyász, kardiológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Belgyógyászat Kutatócsoport
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3.

001-es BibID:BIBFORM061878
Első szerző:Becs Gergely
Cím:Pharmacological induction of ferritin prevents osteoblastic transformation of smooth muscle cells / Gergely Becs, Abolfazl Zarjou, Anupam Agarwal, Katalin Éva Kovács, Ádám Becs, Mónika Nyitrai, Enikő Balogh, Emese Bányai, John W. Eaton, Paolo Arosio, Maura Poli, Viktória Jeney, József Balla, György Balla
Dátum:2016
ISSN:1582-1838
Megjegyzések:Vascular calcification is a frequent complication of atherosclerosis, diabetes and chronic kidney disease. In the latter group of patients, calcification is commonly seen in tunica media where smooth muscle cells (SMC) undergo osteoblastic transformation. Risk factors such as elevated phosphorus levels and vitamin D3 analogues have been identified. In the light of earlier observations by our group and others, we sought to inhibit SMC calcification via induction of ferritin. Human aortic SMC were cultured using b-glycerophosphate with activated vitamin D3, or inorganic phosphate with calcium, and induction of alkaline phosphatase (ALP) and osteocalcin as well as accumulation of calcium were used to monitor osteoblastic transformation. In addition, to examine the role of vitamin D3 analogues, plasma samples from patients on haemodialysis who had received calcitriol or paricalcitol were tested for their tendency to induce calcification of SMC. Addition of exogenous ferritin mitigates the transformation of SMC into osteoblast-like cells. Importantly, pharmacological induction of heavy chain ferritin by 3H-1,2-Dithiole-3-thione was able to inhibit the SMC transition into osteoblast-like cells and calcification of extracellular matrix. Plasma samples collected from patients after the administration of activated vitamin D3 caused significantly increased ALP activity in SMC compared to the samples drawn prior to activated vitamin D3 and here, again induction of ferritin diminished the osteoblastic transformation. Our data suggests that pharmacological induction of ferritin prevents osteoblastic transformation of SMC. Hence, utilization of such agents that will cause enhanced ferritin synthesis may have important clinical applications in prevention of vascular calcification.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
ferritin
ferroxidase activity
[béta]-glycerophosphate
vascular calcification
vitamin D3
Megjelenés:Journal Of Cellular And Molecular Medicine. - 20 : 2 (2016), p. 217-230. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Sikura Katalin Éva (1985-) (biológus) Becs Ádám Nyitrai Mónika Balogh Enikő (1987-) (molekuláris biológus) Bányai Emese (1984-) (orvos) Eaton, John W. Arosio, Paolo Poli, Maura Jeney Viktória (1971-) (vegyész, kémia tanár) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Belgyógyászat Kutatócsoport
K-112333(B.J.)
OTKA
MTA-DE
MTA
Vascularis Biológia, Thrombosis-Haemostasis Kutatócsoport
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4.

001-es BibID:BIBFORM059550
Első szerző:Bolisetty, Subhashini
Cím:Macrophage and epithelial cell H-ferritin expression regulates renal inflammation / Subhashini Bolisetty, Abolfazl Zarjou, Travis D. Hull, Amie M. Traylor, Anjana Perianayagam, Reny Joseph, Ahmed I. Kamal, Paolo Arosio, Miguel P. Soares, Viktoria Jeney, Jozsef Balla, James F. George, Anupam Agarwal
Dátum:2015
ISSN:0085-2538
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
acute kidney injury
ferritin
fibrosis
inflammation
macrophage polarization
Megjelenés:Kidney International. - 88 : 1 (2015), p. 95-108. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Hull, Travis D. Traylor, Amie M. Perianayagam, Anjana Joseph, Reny Kamal, Ahmed I. Arosio, Paolo Soares, Miguel P. Jeney Viktória (1971-) (vegyész, kémia tanár) Balla József (1959-) (belgyógyász, nephrológus) George, James F. Agarwal, Anupam
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5.

001-es BibID:BIBFORM051960
Első szerző:Bolisetty, Subhashini
Cím:Mitochondria-targeted heme oxygenase-1 decreases oxidative stress in renal epithelial cells / Subhashini Bolisetty, Amie Traylor, Abolfazl Zarjou, Michelle S. Johnson, Gloria A. Benavides, Karina Ricart, Ravindra Boddu, Ray D. Moore, Aimee Landar, Stephen Barnes, Victor Darley-Usmar, Anupam Agarwal
Dátum:2013
ISSN:1931-857X 1522-1466
Megjegyzések:Mitochondria are both a source and target of the actions of reactive oxygen species and possess a complex system of inter-related antioxidants that control redox signaling and protect against oxidative stress. Interestingly, the antioxidant enzyme heme oxygenase-1 (HO-1) is not present in the mitochondria despite the fact that the organelle is the site of heme synthesis and contains multiple heme proteins. Detoxification of heme is an important protective mechanism since the reaction of heme with hydrogen peroxide generates pro-oxidant ferryl species capable of propagating oxidative stress and ultimately cell death. We therefore hypothesized that a mitochondrially localized HO-1 would be cytoprotective. To test this, we generated a mitochondria-targeted HO-1 cell line by transfecting HEK293 cells with a plasmid construct containing the manganese superoxide dismutase mitochondria leader sequence fused to HO-1 cDNA (Mito-HO-1). Nontargeted HO-1-overexpressing cells were generated by transfecting HO-1 cDNA (HO-1) or empty vector (Vector). Mitochondrial localization of HO-1 with increased HO activity in the mitochondrial fraction of Mito-HO-1 cells was observed, but a significant decrease in the expression of heme-containing proteins occurred in these cells. Both cytosolic HO-1- and Mito-HO-1-expressing cells were protected against hypoxia-dependent cell death and loss of mitochondrial membrane potential, but these effects were more pronounced with Mito-HO-1. Furthermore, decrement in production of tricarboxylic acid cycle intermediates following hypoxia was significantly mitigated in Mito-HO-1 cells. These data suggest that specific mitochondrially targeted HO-1 under acute pathological conditions may have beneficial effects, but the selective advantage of long-term expression is constrained by a negative impact on the synthesis of heme-containing mitochondrial proteins.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Renal Physiology. - 305 : 3 (2013), p. F255-F264. -
További szerzők:Traylor, Amie Zarjou, Abolfazl (1979-) (kutató orvos) Johnson, Michelle S. Benavides, Gloria A. Ricart, Karina Boddu, Ravindra Moore, Ray D. Landar, Aimee Barnes, Stephen Darley-Usmar, Victor Agarwal, Anupam
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6.

001-es BibID:BIBFORM048367
Első szerző:Czifra Árpád (belgyógyász)
Cím:Hemodialysis and hemodiafiltration differently modulate left ventricular diastolic function / Árpád Czifra, Alida Páll, Julianna Kulcsár, Kitti Barta, Attila Kertész, György Paragh, István Lőrincz, Zoltán Jenei, Anupam Agarwal, Abolfazl Zarjou, József Balla, Zoltán Szabó
Dátum:2013
ISSN:1471-2369
Megjegyzések:Background: Renal replacement therapy may have a favorable effect on diastolic left ventricular function, but it isnot clear whether hemodiafiltration is superior to hemodialysis in this field. Nitric oxide (NO) and asymmetric dimethylarginine (ADMA) may play a role in the changes of intracardiac hemodynamics, but it is not clear whether the different renal replacement methods have disparate influence on the metabolism of these materials.Methods: Thirty patients on renal replacement therapy were investigated. First, data was analyzed while patientsreceived hemodiafiltration over a period of three months. Then, the same patients were evaluated during treatmentwith hemodialysis for at least another three months. Echocardiography was performed before and after renalreplacement therapy.Results: No significant difference was found in the volume removals between hemodialysis and hemodiafiltration.The left atrial diameter and transmitral flow velocities (E/A) decreased significantly only during hemodiafiltration. A positive correlation was observed between the left atrial diameter and E/Ea representing the left ventricular pressure load during hemodiafiltration. Significant correlations between NO and A and E/A were observed only in the case of hemodiafiltration.Conclusion: Hemodiafiltration has a beneficial effect on echocardiographic markers representing left ventriculardiastolic function. This could be attributed to the differences between the dynamics of volume removal and itsdistribution among liquid compartments.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Hemodiafiltration
Hemodialysis
Echocardiography
Diastolic function
Nitric oxide
Megjelenés:BMC Nephrology. - 14 : 1 (2013), p. 1-7. -
További szerzők:Páll Alida (1983-) (orvos) Kulcsár Júlia (1983-) (orvos) Barta Kitti (1977-) (belgyógyász) Kertész Attila Béla (1973-) (kardiológus) Paragh György (1953-) (belgyógyász) Lőrincz István (1950-) (belgyógyász, kardiológus) Jenei Zoltán (1968-) (belgyógyász) Agarwal, Anupam Zarjou, Abolfazl (1979-) (kutató orvos) Balla József (1959-) (belgyógyász, nephrológus) Szabó Zoltán (1973-) (belgyógyász, kardiológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
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7.

001-es BibID:BIBFORM025266
Első szerző:Jeney Viktória (vegyész, kémia tanár)
Cím:Ferritin/Ferroxidase Activity : a Potent Inhibitor of Vascular Calcification, Osteoblastic Transdifferentiation of Vascular Smooth Muscle Cells and Osteoblast Activity / Viktória Jeney, Abolfazl Zarjou, Paolo Arosio, Maura Poli, Anupam Agarwal, György Balla, József Balla
Dátum:2011
ISBN:978 1 61942 347 3
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Megjelenés:Ferritin: Functions, Byosynthesis and Regulation / eds. Gael Soto da Lima, Marco F. Azevedo Cabral. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Arosio, Paolo Poli, Maura Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:TÁMOP-4.2.1./B-09/1/KONV-2010-0007
TÁMOP
Haemostasis thrombosis és vascularis biológia
OTKA-K75883
OTKA
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8.

001-es BibID:BIBFORM051966
Első szerző:Kim, Junghyun
Cím:In vivo regulation of the heme oxygenase-1 gene in humanized transgenic mice / Junghyun Kim, Abolfazl Zarjou, Amie M. Traylor, Subhashini Bolisetty, Edgar A. Jaimes, Travis D. Hull, James F. George, Fady M. Mikhail, Anupam Agarwal
Dátum:2012
ISSN:0085-2538
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Kidney International. - 82 : 3 (2012), p. 278-291. -
További szerzők:Zarjou, Abolfazl (1979-) (kutató orvos) Traylor, Amie M. Bolisetty, Subhashini Jaimes, Edgar A. Hull, Travis D. George, James F. Mikhail, Fady M. Agarwal, Anupam
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9.

001-es BibID:BIBFORM083275
035-os BibID:(cikkazonosító)1584 (WoS)000509956400001 (Scopus)85078738706
Első szerző:Nagy Annamária
Cím:Zinc Inhibits HIF-Prolyl Hydroxylase Inhibitor-Aggravated VSMC Calcification Induced by High Phosphate / Annamária Nagy, Dávid Pethő, Tamás Gáll, Erzsébet Zavaczki, Mónika Nyitrai, József Posta, Abolfazl Zarjou, Anupam Agarwal, György Balla, József Balla
Dátum:2020
ISSN:1664-042X
Megjegyzések:Vascular calcification is a life-threatening clinical condition in chronic kidney disease (CKD) and is associated with reduced zinc serum levels. Anemia is another frequent complication of CKD. Hypoxia-inducible factor (HIF) stabilizers, also known as HIF prolyl hydroxylase inhibitors (PHI), are promising candidates to treat CKD-associated anemia by increasing erythropoietin synthesis. Recent evidence suggests that HIFs play a pivotal role in vascular calcification. Our study explored feasible impacts of HIF PHI on phosphate (Pi)-induced calcification of vascular smooth muscle cells (VSMCs) and tested whether zinc might inhibit this mineralization process. Treatment of VSMCs with PHI aggravated Pi-induced calcium deposition and Pi uptake. PHI promoted Pi-induced loss of smooth muscle cell markers (ACTA-2, MYH11, SM22?) and enhanced osteochondrogenic gene expression (Msx-2, BMP-2, Sp7) triggering osteochondrogenic phenotypic switch of VSMCs. These effects of PHI paralleled with increased pyruvate dehydrogenase kinase 4 (PDK4) expression, decreased Runx2 Ser451 phosphorylation, and reduced cell viability. Zinc inhibited Pi-induced mineralization of VSMCs in a dose-dependent manner and also attenuated the pro-calcification effect of PHI in Pi-induced mineralization. Zinc inhibited osteochondrogenic phenotypic switch of VSMCs reflected by lowering Pi uptake, decreasing the expressions of Msx-2, BMP-2, and Sp7 as well as the loss of smooth muscle cell-specific markers. Zinc preserved phosphorylation state of Runx2 Ser451, decreased PDK4 level, and restored cell viability. PHI alone reduced the expression of smooth muscle markers without inducing mineralization, which was also inhibited by zinc. In addition, we observed a significantly lower serum zinc level in CKD as well as in patients undergoing carotid endarterectomy compared to healthy individuals. Conclusion - PHI promoted the loss of smooth muscle markers and augmented Pi-induced osteochondrogenic phenotypic switch leading to VSMCs calcification. This mineralization process was attenuated by zinc. Enhanced vascular calcification is a potential risk factor during PHI therapy in CKD which necessitates the strict follow up of vascular calcification and zinc supplementation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
vascular calcification, PHI
Megjelenés:Frontiers in Physiology. - 10 (2020), p. 1-15. -
További szerzők:Pethő Dávid Gáll Tamás (1982-) (molekuláris biológus, mikrobiológus) Zavaczki Erzsébet (1983-) (biotechnológus) Nyitrai Mónika Posta József (1948-) (vegyész, analitikus) Zarjou, Abolfazl (1979-) (kutató orvos) Agarwal, Anupam Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Balla József (1959-) (belgyógyász, nephrológus)
Pályázati támogatás:OTKA-112333
OTKA
K132828
OTKA
GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
EFOP-3.6.3-VEKOP16-2017-00009
EFOP
ED-18-1-2019-0028
Egyéb
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10.

001-es BibID:BIBFORM061017
Első szerző:Páll Alida (orvos)
Cím:Hemodiafiltration and hemodialysis differently affect P wave duration and dispersion on the surface electrocardiogram / Alida Páll, Árpád Czifra, Veronika Sebestyén, Gergely Becs, Csaba Kun, József Balla, György Paragh, István Lőrincz, Dénes Páll, János Tamás Padra, Anupam Agarwal, Abolfazl Zarjou, Zoltán Szabó
Dátum:2016
ISSN:0301-1623
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Urology And Nephrology 48 : 2 (2016), p. 271-277. -
További szerzők:Czifra Árpád (1983-) (belgyógyász) Borbásné Sebestyén Veronika (1990-) (biofizikus) Becs Gergely Kun Csaba (1969-) (kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Paragh György (1953-) (belgyógyász) Lőrincz István (1950-) (belgyógyász, kardiológus) Páll Dénes (1967-) (belgyógyász, kardiológus) Padra János Tamás (1984-) (biológus) Agarwal, Anupam Zarjou, Abolfazl (1979-) (kutató orvos) Szabó Zoltán (1973-) (belgyógyász, kardiológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
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11.

001-es BibID:BIBFORM078365
035-os BibID:(WoS)000461679000073 (Scopus)85063288166 (PMID)30833408
Első szerző:Ramos, Susana
Cím:Renal control of disease tolerance to malaria / Susana Ramos, Ana Rita Carlos, Balamurugan Sundaram, Viktoria Jeney, Ana Ribeiro, Raffaella Gozzelino, Claudia Bank, Erida Gjini, Faouzi Braza, Rui Martins, Temitope Wilson Ademolue, Birte Blankenhaus, Zélia Gouveia, Pedro Faísca, Damian Trujillo, Sílvia Cardoso, Sofia Rebelo, Laura del Barrio, Abolfazl Zarjou, Subhashini Bolisetty, Anupam Agarwal, Miguel P. Soares
Dátum:2019
ISSN:0027-8424 1091-6490
Megjegyzések:Malaria, the disease caused by Plasmodium spp. infection, remains a major global cause of morbidity and mortality. Host protection from malaria relies on immune-driven resistance mechanisms that kill Plasmodium However, these mechanisms are not sufficient per se to avoid the development of severe forms of disease. This is accomplished instead via the establishment of disease tolerance to malaria, a defense strategy that does not target Plasmodium directly. Here we demonstrate that the establishment of disease tolerance to malaria relies on a tissue damage-control mechanism that operates specifically in renal proximal tubule epithelial cells (RPTEC). This protective response relies on the induction of heme oxygenase-1 (HMOX1; HO-1) and ferritin H chain (FTH) via a mechanism that involves the transcription-factor nuclear-factor E2-related factor-2 (NRF2). As it accumulates in plasma and urine during the blood stage of Plasmodium infection, labile heme is detoxified in RPTEC by HO-1 and FTH, preventing the development of acute kidney injury, a clinical hallmark of severe malaria.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
disease tolerance
heme
infection
kidney
malaria
Megjelenés:Proceedings of the National Academy of Sciences of the United States of America. - 116 : 12 (2019), p. 5681-5686. -
További szerzők:Carlos, Ana Rita Sundaram, Balamurugan Jeney Viktória (1971-) (vegyész, kémia tanár) Ribeiro, Ana Gozzelino, Raffaella Bank, Claudia Gjini, Erida Braza, Faouzi Martins, Rui Ademolue, Temitope Wilson Blankenhaus, Birte Gouveia, Zélia Faísca, Pedro Trujillo, Damian Cardoso, Sílvia Rebelo, Sofia del Barrio, Laura Zarjou, Abolfazl (1979-) (kutató orvos) Bolisetty, Subhashini Agarwal, Anupam Soares, Miguel P.
Pályázati támogatás:OTKA-116024
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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12.

001-es BibID:BIBFORM051963
Első szerző:Schoeb, Trenton R.
Cím:Endothelial nitric oxide synthase inhibits the development of autoimmune-mediated vasculitis in mice / Trenton R. Schoeb, Tambi Jarmi, M. John Hicks, Scott Henke, Abolfazl Zarjou, Hitoshi Suzuki, Philip Kramer, Jan Novak, Anupam Agarwal, Daniel C. Bullard
Dátum:2012
ISSN:0004-3591
Megjegyzések:OBJECTIVE: Many different genes or mediators have been implicated in promoting the development of vasculitis, although little is known regarding the mechanisms that normally act to suppress lesion formation. Endothelial nitric oxide synthase (eNOS) has been shown to inhibit vascular inflammation in many different model systems, but its roles in the pathogenesis of vasculitis have not been elucidated. This study was undertaken to determine the functions of eNOS in the initiation and progression of vasculitic lesion formation. METHODS: MRL/MpJ-Fas(lpr) mice lacking the gene for eNOS (Nos3(-/-) ) were generated and comprehensively evaluated and compared to controls with regard to the development of autoimmune disease, including vasculitic lesion formation and glomerulonephritis. RESULTS: Nos3(-/-) MRL/MpJ-Fas(lpr) mice exhibited accelerated onset and increased incidence of renal vasculitis compared to Nos3(+/+) controls. In contrast, no significant differences in severity of glomerulonephritis were observed between groups. Vasculitis was also observed in other organs of eNOS-deficient mice, including in the lungs of several of these animals. Ultrastructural analyses of renal lesions revealed the presence of electron-dense deposits in affected arteries, and IgG, IgA, and C3 deposition was observed in some vessels in the kidneys of Nos3(-/-) mice. In addition, Nos3(-/-) MRL/MpJ-Fas(lp) mice showed increased levels of circulating IgG-IgA immune complexes at 20 weeks of age, compared to Nos3(+/+) MRL/MpJ-Fas(lpr) and Nos3(-/-) C57BL/6 mice. CONCLUSION: These findings strongly indicate that eNOS serves as a negative regulator of vasculitis in MRL/MpJ-Fas(lpr) mice and further suggest that NO produced by this enzyme may be critical for inhibiting lesion formation and vascular damage in human vasculitic diseases.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis And Rheumatism. - 64 : 12 (2012), p. 4114-4124. -
További szerzők:Jarmi, Tambi Hicks, M. John Henke, Scott Zarjou, Abolfazl (1979-) (kutató orvos) Suzuki, Hitoshi Kramer, Philip Novak, Jan Agarwal, Anupam Bullard, Daniel C.
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