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Article: Learning and assessment strategies to develop specific and transversal competencies for a humanized medical education.

Tutor, Antonio S / Escudero, Esther / Del Nogal Ávila, María / Aranda, Juan Francisco / Torres, Hortensia / Yague, Josué G / Borrego, María José / Muñoz, Úrsula / Sádaba, María C / Sánchez-Vera, Isabel

Frontiers in physiology

2023 Volume 14, Page(s) 1212031

Abstract: Introduction: ...

Abstract	Introduction:
Language	English
Publishing date	2023-07-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1212031
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Article ; Online: Cytokine storm-based mechanisms for extrapulmonary manifestations of SARS-CoV-2 infection.

Del Nogal Avila, Maria / Das, Ranjan / Kharlyngdoh, Joubert / Molina-Jijon, Eduardo / Donoro Blazquez, Hector / Gambut, Stéphanie / Crowley, Michael / Crossman, David K / Gbadegesin, Rasheed A / Chugh, Sunveer S / Chugh, Sunjeet S / Avila-Casado, Carmen / Macé, Camille / Clement, Lionel C / Chugh, Sumant S

JCI insight

2023 Volume 8, Issue 10

Abstract: Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus ... ...

Abstract	Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus common cold infection. At low doses, COVID-19 cocktails induced glomerular injury and albuminuria in zinc fingers and homeoboxes 2 (Zhx2) hypomorph and Zhx2+/+ mice to mimic COVID-19-related proteinuria. Common Cold cocktail induced albuminuria selectively in Zhx2 hypomorph mice to model relapse of minimal change disease, which improved after depletion of TNF-α, soluble IL-4Rα, or IL-6. The Zhx2 hypomorph state increased cell membrane to nuclear migration of podocyte ZHX proteins in vivo (both cocktails) and lowered phosphorylated STAT6 activation (COVID-19 cocktail) in vitro. At higher doses, COVID-19 cocktails induced acute heart injury, myocarditis, pericarditis, acute liver injury, acute kidney injury, and high mortality in Zhx2+/+ mice, whereas Zhx2 hypomorph mice were relatively protected, due in part to early, asynchronous activation of STAT5 and STAT6 pathways in these organs. Dual depletion of cytokine combinations of TNF-α with IL-2, IL-13, or IL-4 in Zhx2+/+ mice reduced multiorgan injury and eliminated mortality. Using genome sequencing and CRISPR/Cas9, an insertion upstream of ZHX2 was identified as a cause of the human ZHX2 hypomorph state.
MeSH term(s)	Humans ; Mice ; Animals ; Homeodomain Proteins/genetics ; Albuminuria ; Tumor Necrosis Factor-alpha ; Common Cold ; Cytokine Release Syndrome ; COVID-19 ; SARS-CoV-2/metabolism ; Transcription Factors/genetics
Chemical Substances	Homeodomain Proteins ; Tumor Necrosis Factor-alpha ; ZHX2 protein, human ; Transcription Factors
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.166012
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Article: Angiopoietin-like 4 based therapeutics for proteinuria and kidney disease.

Chugh, Sumant S / Macé, Camille / Clement, Lionel C / Del Nogal Avila, Maria / Marshall, Caroline B

Frontiers in pharmacology

2014 Volume 5, Page(s) 23

Abstract: Current drugs used to treat proteinuric disorders of the kidney have been borrowed from other branches of medicine, and are only partially effective. The discovery of a central, mechanistic role played by two different forms of the secreted glycoprotein ... ...

Abstract	Current drugs used to treat proteinuric disorders of the kidney have been borrowed from other branches of medicine, and are only partially effective. The discovery of a central, mechanistic role played by two different forms of the secreted glycoprotein angiopoietin-like 4 (Angptl4) in human and experimental glomerular disease has opened new treatment avenues. Localized upregulation of a hyposialylated form (lacks sialic acid residues) of Angptl4 secreted by podocytes induces the cardinal morphological and clinical manifestations of human minimal change disease, and is also being increasingly recognized as a significant contributor toward proteinuria in experimental diabetic nephropathy. Oral treatment with low doses of N-acetyl-D-mannosamine, a naturally occurring precursor of sialic acid, improves sialylation of Angptl4 in vivo, and reduces proteinuria by over 40%. By contrast, a sialylated circulating form of Angptl4, mostly secreted from skeletal muscle, heart and adipose tissue in all major primary glomerular diseases, reduces proteinuria while also causing hypertriglyceridemia. Intravenous administration of recombinant human Angptl4 mutated to avoid hypertriglyceridemia and cleavage has remarkable efficacy in reducing proteinuria by as much as 65% for 2 weeks after a single low dose. Both interventions are mechanistically relevant, utilize naturally occurring pathways, and represent new generation therapeutic agents for chronic kidney disease related to glomerular disorders.
Language	English
Publishing date	2014-02-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2014.00023
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Article ; Online: The proteinuria-hypertriglyceridemia connection as a basis for novel therapeutics for nephrotic syndrome.

Clement, Lionel C / Macé, Camille / Del Nogal Avila, Maria / Marshall, Caroline B / Chugh, Sumant S

Translational research : the journal of laboratory and clinical medicine

2014 Volume 165, Issue 4, Page(s) 499–504

Abstract: The development of new and specific treatment options for kidney disease in general and glomerular diseases in specific has lagged behind other fields like heart disease and cancer. As a result, nephrologists have had to test and adapt therapeutics ... ...

Abstract	The development of new and specific treatment options for kidney disease in general and glomerular diseases in specific has lagged behind other fields like heart disease and cancer. As a result, nephrologists have had to test and adapt therapeutics developed for other indications to treat glomerular diseases. One of the major factors contributing to this inertia has been the poor understanding of disease mechanisms. One way to elucidate these disease mechanisms is to study the association between the cardinal manifestations of glomerular diseases. Because many of these patients develop nephrotic syndrome, understanding the relationship of proteinuria, the primary driver in this syndrome, with hypoalbuminemia, hypercholesterolemia, hypertriglyceridemia, edema, and lipiduria could provide valuable insight. The recent unraveling of the relationship between proteinuria and hypertriglyceridemia mediated by free fatty acids, albumin, and the secreted glycoprotein angiopoietin-like 4 (Angptl4) offers a unique opportunity to develop novel therapeutics for glomerular diseases. In this review, the therapeutic potential of mutant forms of Angptl4 in reducing proteinuria and, as a consequence, alleviating the other manifestations of nephrotic syndrome is discussed.
MeSH term(s)	Angiopoietin-Like Protein 4 ; Angiopoietins/genetics ; Angiopoietins/pharmacology ; Humans ; Hypertriglyceridemia/complications ; Nephrotic Syndrome/drug therapy ; Nephrotic Syndrome/etiology ; Proteinuria/complications ; Recombinant Proteins
Chemical Substances	ANGPTL4 protein, human ; Angiopoietin-Like Protein 4 ; Angiopoietins ; Recombinant Proteins
Language	English
Publishing date	2014-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2014.06.004
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Article ; Online: Novel therapeutic approaches for chronic kidney disease due to glomerular disorders.

Del Nogal-Avila, Maria / Donoro-Blazquez, Hector / Saha, Manish K / Marshall, Caroline B / Clement, Lionel C / Macé, Camille E A / Chugh, Sumant S

American journal of physiology. Renal physiology

2016 Volume 311, Issue 1, Page(s) F63–5

Abstract: Improved understanding of glomerular disease mechanisms over the past decade has led to the emergence of new and targeted therapeutic strategies for chronic kidney disease (CKD). Most promising among these are the administration of recombinant mutated ... ...

Abstract	Improved understanding of glomerular disease mechanisms over the past decade has led to the emergence of new and targeted therapeutic strategies for chronic kidney disease (CKD). Most promising among these are the administration of recombinant mutated human angiopoietin-like 4, sialic acid-related sugars that induce sialylation in vivo, compounds related to Bis-T-23, and immune depletion of the soluble urokinase receptor from the circulation. Taking these therapeutic strategies into clinical trials will be the first step away from repurposed and relatively toxic drugs currently used for treating kidney disease.
MeSH term(s)	Angiopoietin-like 4 Protein ; Angiopoietins/therapeutic use ; Animals ; Humans ; Kidney Glomerulus/pathology ; Proteinuria/drug therapy ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/pathology
Chemical Substances	ANGPTL4 protein, human ; Angiopoietin-like 4 Protein ; Angiopoietins
Language	English
Publishing date	2016-07-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00245.2016
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Article ; Online: The zinc fingers and homeoboxes 2 protein ZHX2 and its interacting proteins regulate upstream pathways in podocyte diseases.

Macé, Camille / Del Nogal Avila, Maria / Marshall, Caroline B / Kharlyngdoh, Joubert / Das, Ranjan / Molina-Jijon, Eduardo / Donoro Blazquez, Hector / Shastry, Suresh / Soria, Elisabeth / Wetzels, Jack / Dijkman, Henry / Avila-Casado, Carmen / Clement, Lionel C / Chugh, Sumant S

Kidney international

2019 Volume 97, Issue 4, Page(s) 753–764

Abstract: Zinc fingers and homeoboxes (ZHX) proteins are heterodimeric transcriptional factors largely expressed at the cell membrane in podocytes in vivo. We found ZHX2-based heterodimers in podocytes, with ZHX2-ZHX1 predominantly at the cell membrane of the ... ...

Abstract	Zinc fingers and homeoboxes (ZHX) proteins are heterodimeric transcriptional factors largely expressed at the cell membrane in podocytes in vivo. We found ZHX2-based heterodimers in podocytes, with ZHX2-ZHX1 predominantly at the cell membrane of the podocyte cell body, and ZHX2-ZHX3 at the slit diaphragm. In addition to changes in overall ZHX2 expression, there was increased podocyte nuclear ZHX3 and ZHX2 in patients with focal segmental glomerulosclerosis, and increased podocyte nuclear ZHX1 in patients with minimal change disease. Zhx2 deficient mice had increased podocyte ZHX1 and ZHX3 expression. Zhx2 deficient mice and podocyte specific Zhx2 overexpressing transgenic rats develop worse experimental focal segmental glomerulosclerosis than controls, with increased nuclear ZHX3 and ZHX2, respectively. By contrast, podocyte specific Zhx2 overexpressing transgenic rats develop lesser proteinuria during experimental minimal change disease due to peripheral sequestration of ZHX1 by ZHX2. Using co-immunoprecipitation, the interaction of ZHX2 with aminopeptidase A in the podocyte body cell membrane, and EPHRIN B1 in the slit diaphragm were noted to be central to upstream events in animal models of minimal change disease and focal segmental glomerulosclerosis, respectively. Mice deficient in Enpep, the gene for aminopeptidase A, and Efnb1, the gene for ephrin B1 developed worse albuminuria in glomerular disease models. Targeting aminopeptidase A in Zhx2 deficient mice with monoclonal antibodies induced albuminuria and upregulation of the minimal change disease mediator angiopoietin-like 4 through nuclear entry of ZHX1. Thus, podocyte ZHX2 imbalance is a critical factor in human glomerular disease, with minimal change disease disparities mediated mostly through ZHX1, and focal segmental glomerulosclerosis deviations through ZHX3 and ZHX2.
MeSH term(s)	Animals ; Genes, Homeobox ; Glomerulosclerosis, Focal Segmental/genetics ; Homeodomain Proteins/genetics ; Humans ; Mice ; Podocytes/metabolism ; Transcription Factors/genetics ; Zinc Fingers
Chemical Substances	Homeodomain Proteins ; Transcription Factors ; ZHX2 protein, human
Language	English
Publishing date	2019-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2019.11.011
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Article ; Online: Corrigendum to "Glucose Oxidase Induces Cellular Senescence in Immortal Renal Cells through ILK by Downregulating

Troyano-Suárez, Nuria / Del Nogal-Avila, María / Mora, Inés / Sosa, Patricia / López-Ongil, Susana / Rodriguez-Puyol, Diego / Olmos, Gemma / Ruíz-Torres, María Piedad

Oxidative medicine and cellular longevity

2016 Volume 2016, Page(s) 8392708

Abstract: This corrects the article DOI: 10.1155/2015/416738.]. ...

Abstract	[This corrects the article DOI: 10.1155/2015/416738.].
Language	English
Publishing date	2016
Publishing country	United States
Document type	Published Erratum
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2016/8392708
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Article ; Online: Glucose Oxidase Induces Cellular Senescence in Immortal Renal Cells through ILK by Downregulating Klotho Gene Expression.

Troyano-Suárez, Nuria / del Nogal-Avila, María / Mora, Inés / Sosa, Patricia / López-Ongil, Susana / Rodriguez-Puyol, Diego / Olmos, Gemma / Ruíz-Torres, María Piedad

Oxidative medicine and cellular longevity

2015 Volume 2015, Page(s) 416738

Abstract: Cellular senescence can be prematurely induced by oxidative stress involved in aging. In this work, we were searching for novel intermediaries in oxidative stress-induced senescence, focusing our interest on integrin-linked kinase (ILK), a scaffold ... ...

Abstract	Cellular senescence can be prematurely induced by oxidative stress involved in aging. In this work, we were searching for novel intermediaries in oxidative stress-induced senescence, focusing our interest on integrin-linked kinase (ILK), a scaffold protein at cell-extracellular matrix (ECM) adhesion sites, and on the Klotho gene. Cultured renal cells were treated with glucose oxidase (GOx) for long time periods. GOx induced senescence, increasing senescence associated β-galactosidase activity and the expression of p16. In parallel, GOx increased ILK protein expression and activity. Ectopic overexpression of ILK in cells increased p16 expression, even in the absence of GOx, whereas downregulation of ILK inhibited the increase in p16 due to oxidative stress. Additionally, GOx reduced Klotho gene expression and cells overexpressing Klotho protein did not undergo senescence after GOx addition. We demonstrated a direct link between ILK and Klotho since silencing ILK expression in cells and mice increases Klotho expression and reduces p53 and p16 expression in renal cortex. In conclusion, oxidative stress induces cellular senescence in kidney cells by increasing ILK protein expression and activity, which in turn reduces Klotho expression. We hereby present ILK as a novel downregulator of Klotho gene expression.
MeSH term(s)	Animals ; Cells, Cultured ; Cellular Senescence/drug effects ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Down-Regulation/drug effects ; Glucose Oxidase/pharmacology ; Glucuronidase/genetics ; Glucuronidase/metabolism ; HEK293 Cells ; Humans ; Kidney Tubules/cytology ; Kidney Tubules/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA Interference ; Transfection ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16 ; Tumor Suppressor Protein p53 ; Glucose Oxidase (EC 1.1.3.4) ; integrin-linked kinase (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2015/416738
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Article ; Online: Amadori products promote cellular senescence activating insulin-like growth factor-1 receptor and down-regulating the antioxidant enzyme catalase.

Del Nogal-Ávila, María / Troyano-Suárez, Nuria / Román-García, Pablo / Cannata-Andía, Jorge B / Rodriguez-Puyol, Manuel / Rodriguez-Puyol, Diego / Kuro-O, Makoto / Ruiz-Torres, María P

The international journal of biochemistry & cell biology

2013 Volume 45, Issue 7, Page(s) 1255–1264

Abstract: Activation of the insulin growth factor receptor-1 signaling pathways has been largely related to the aging process. Amadori products are produced in pathological conditions such as diabetes and aging, and are potentially involved in diabetic nephropathy ...

Abstract	Activation of the insulin growth factor receptor-1 signaling pathways has been largely related to the aging process. Amadori products are produced in pathological conditions such as diabetes and aging, and are potentially involved in diabetic nephropathy or age-associated decline of renal function. We hypothesize that Amadori products induce senescence in primary human mesangial cells through the activation of IGF-1 receptor and investigate, in the present work, the intracellular mechanism involved after this activation. We treated cultured human mesangial cells with glycated albumin, one of the most abundant Amadori product, and senescence was assessed by determining the senescence associated β-galactosidase activity and the expression of the cell cycle regulators p53 and p21. We demonstrated that prolonged exposition (more than 24h) to glycated albumin induced senescence and, in parallel, incremented the release of IGF-1 and the activation of the IGF-1 receptor. Inhibition of the IGF-1 activation prevented the GA induced senescence. Activation of IGF-1R, after GA addition, promoted a reduction in the catalase content through the constitutive activation of Ras and erk1/2 proteins which were, in turn, responsible of the observed GA-induced senescence. In conclusion, we propose that the Amadori product, glycated albumin, promotes premature cell senescence in mesangial cells through the activation of the IGF-1 receptor and the subsequent reduction in the antioxidant enzyme catalase.
MeSH term(s)	Catalase/biosynthesis ; Cells, Cultured ; Cellular Senescence/physiology ; Down-Regulation ; Glomerular Mesangium/cytology ; Glomerular Mesangium/metabolism ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mesangial Cells/metabolism ; Receptor, IGF Type 1/metabolism ; Serum Albumin/pharmacology ; Signal Transduction/drug effects ; Tumor Suppressor Protein p53/biosynthesis ; beta-Galactosidase/drug effects ; beta-Galactosidase/metabolism ; rho GTP-Binding Proteins/biosynthesis
Chemical Substances	Serum Albumin ; Tumor Suppressor Protein p53 ; glycated serum albumin ; Insulin-Like Growth Factor I (67763-96-6) ; Catalase (EC 1.11.1.6) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; beta-Galactosidase (EC 3.2.1.23) ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2013-04-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2013.03.018
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Article: Amadori products promote cellular senescence activating insulin-like growth factor-1 receptor and down-regulating the antioxidant enzyme catalase

del Nogal-Ávila, María / Troyano-Suárez, Nuria / Román-García, Pablo / Cannata-Andía, Jorge B. / Rodriguez-Puyol, Manuel / Rodriguez-Puyol, Diego / Kuro-O, Makoto / Ruiz-Torres, María P.

international journal of biochemistry & cell biology

Volume v. 45,, Issue no. 7

Abstract	Activation of the insulin growth factor receptor-1 signaling pathways has been largely related to the aging process. Amadori products are produced in pathological conditions such as diabetes and aging, and are potentially involved in diabetic nephropathy or age-associated decline of renal function. We hypothesize that Amadori products induce senescence in primary human mesangial cells through the activation of IGF-1 receptor and investigate, in the present work, the intracellular mechanism involved after this activation. We treated cultured human mesangial cells with glycated albumin, one of the most abundant Amadori product, and senescence was assessed by determining the senescence associated β-galactosidase activity and the expression of the cell cycle regulators p53 and p21. We demonstrated that prolonged exposition (more than 24h) to glycated albumin induced senescence and, in parallel, incremented the release of IGF-1 and the activation of the IGF-1 receptor. Inhibition of the IGF-1 activation prevented the GA induced senescence. Activation of IGF-1R, after GA addition, promoted a reduction in the catalase content through the constitutive activation of Ras and erk1/2 proteins which were, in turn, responsible of the observed GA-induced senescence. In conclusion, we propose that the Amadori product, glycated albumin, promotes premature cell senescence in mesangial cells through the activation of the IGF-1 receptor and the subsequent reduction in the antioxidant enzyme catalase.
Keywords	insulin-like growth factor I receptor ; renal function ; insulin-like growth factor I ; catalase ; humans ; signal transduction ; cell cycle ; Amadori products ; albumins ; beta-galactosidase ; antioxidants ; diabetic nephropathy ; cell senescence
Language	English
Document type	Article
ISSN	1357-2725
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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