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1.

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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2.

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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3.

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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4.

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
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5.

001-es BibID:BIBFORM077162
035-os BibID:(WoS)000457627800001 (Scopus)85062188852 (cikkazonosító)131
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury / Zarjou Abolfazl, Black Laurence M., McCullough Kayla R., Hull Travis D., Esman Stephanie K., Boddu Ravindra, Varambally Sooryanarayana, Chandrashekar Darshan S., Feng Wenguang, Arosio Paolo, Poli Maura, Balla Jozsef, Bolisetty Subhashini
Dátum:2019
ISSN:1664-3224
Megjegyzések:Despite the prevalence and recognition of its detrimental impact, clinical complications of sepsis remain a major challenge. Here, we investigated the effects of myeloid ferritin heavy chain (FtH) in regulating the pathogenic sequelae of sepsis. We demonstrate that deletion of myeloid FtH leads to protection against lipopolysaccharide-induced endotoxemia and cecal ligation and puncture (CLP)-induced model of sepsis as evidenced by reduced cytokine levels, multi-organ dysfunction and mortality. We identified that such protection is predominantly mediated by the compensatory increase in circulating ferritin (ferritin light chain; FtL) in the absence of myeloid FtH. Our in vitro and in vivo studies indicate that prior exposure to ferritin light chain restrains an otherwise dysregulated response to infection. These findings are mediated by an inhibitory action of FtL on NF-?B activation, a key signaling pathway that is implicated in the pathogenesis of sepsis. We further identified that LPS mediated activation of MAPK pathways, specifically, JNK, and ERK were also reduced with FtL pre-treatment. Taken together, our findings elucidate a crucial immunomodulatory function for circulating ferritin that challenges the traditional view of this protein as a mere marker of body iron stores. Accordingly, these findings will stimulate investigations to the adaptive nature of this protein in diverse clinical settings.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
ferritin
inflammatory response
sepsis
NF-B, cytokine
LPS
multi-organ injury
myeloid cells
Megjelenés:Frontiers in Immunology. - 10 (2019), p. 1-15. -
További szerzők:Black, Laurence M. McCullough, Kayla R. Hull, Travis D. Esman, Stephanie K. Boddu, Ravindra Varambally, Sooryanarayana Chandrashekar, Darshan S. Feng, Wenguang Arosio, Paolo Poli, Maura Balla József (1959-) (belgyógyász, nephrológus) Bolisetty, Subhashini
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6.

001-es BibID:BIBFORM049052
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Proximal tubule H-ferritin mediates iron trafficking in acute kidney injury / Abolfazl Zarjou, Subhashini Bolisetty, Reny Joseph, Amie Traylor, Eugene O. Apostolov, Paolo Arosio, Jozsef Balla, Jill Verlander, Deepak Darshan, Lukas C. Kuhn, Anupam Agarwal
Dátum:2013
ISSN:0021-9738
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Clinical Investigation. - 123 : 10 (2013), p. 4423-4434. -
További szerzők:Bolisetty, Subhashini Joseph, Reny Traylor, Amie Apostolov, Eugene O. Arosio, Paolo Balla József (1959-) (belgyógyász, nephrológus) Verlander, Jill Darshan, Deepak Kuhn, Lukas C. Agarwal, Anupam
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