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Article ; Online: Autophagy and metabolic changes in obesity-related chronic kidney disease.

Satriano, Joseph / Sharma, Kumar

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2013 Volume 28 Suppl 4, Page(s) iv29–36

Abstract: Obesity is a long-term source of cellular stress that predisposes to chronic kidney disease (CKD). Autophagy is a homeostatic mechanism for cellular quality control through the disposal and recycling of cellular components. During times of cellular ... ...

Abstract	Obesity is a long-term source of cellular stress that predisposes to chronic kidney disease (CKD). Autophagy is a homeostatic mechanism for cellular quality control through the disposal and recycling of cellular components. During times of cellular stress, autophagy affords mechanisms to manage stress by selectively ridding the cell of the accumulation of potentially toxic proteins, lipids and organelles. The adaptive processes employed may vary between cell types and selectively adjust to the insult by inducing components of the basic autophagy machinery utilized by the cells while not under duress. In this review, we will discuss the autophagic responses of organs to cellular stressors, such as high-fat diet, obesity and diabetes, and how these mechanisms may prevent or promote the progression of disease. The identification of early cellular mechanisms in the advent of obesity- and diabetes-related renal complications could afford avenues for future therapeutic interventions.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Obesity/complications ; Obesity/metabolism ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/metabolism
Language	English
Publishing date	2013-07-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gft229
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Article: Agmatine: at the crossroads of the arginine pathways.

Satriano, Joseph

Annals of the New York Academy of Sciences

2003 Volume 1009, Page(s) 34–43

Abstract: In acute inflammatory responses, such as wound healing and glomerulonephritis, arginine is the precursor for production of the cytostatic molecule nitric oxide (NO) and the pro-proliferative polyamines. NO is an early phase response whereas increased ... ...

Abstract	In acute inflammatory responses, such as wound healing and glomerulonephritis, arginine is the precursor for production of the cytostatic molecule nitric oxide (NO) and the pro-proliferative polyamines. NO is an early phase response whereas increased generation of polyamines is requisite for the later, repair phase response. The temporal switch of arginine as a substrate for the inducible nitric oxide synthase (iNOS)/NO axis to arginase/ornithine decarboxylase (ODC)/polyamine axis is subject to regulation by inflammatory cytokines as well as interregulation by the arginine metabolites themselves. Herein we describe the capacity of another arginine pathway, the metabolism of arginine to agmatine by arginine decarboxylase (ADC), to aid in this interregulation. Agmatine is an antiproliferative molecule due to its suppressive effects on intracellular polyamine levels, whereas the aldehyde metabolite of agmatine is a potent inhibitor of iNOS. We propose that the catabolism of agmatine to its aldehyde metabolite may act as a gating mechanism at the transition from the iNOS/NO axis to the arginase/ODC/polyamine axis. Thus, agmatine has the potential to serve in the coordination of the early and repair phase pathways of arginine in inflammation.
MeSH term(s)	Agmatine/metabolism ; Animals ; Arginine/metabolism ; Carboxy-Lyases/metabolism ; Humans ; Inflammation/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; Polyamines/metabolism
Chemical Substances	Polyamines ; Nitric Oxide (31C4KY9ESH) ; Agmatine (70J407ZL5Q) ; Arginine (94ZLA3W45F) ; NOS2 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Carboxy-Lyases (EC 4.1.1.-) ; arginine decarboxylase (EC 4.1.1.19)
Language	English
Publishing date	2003-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1196/annals.1304.004
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Article ; Online: Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers.

Declèves, Anne-Emilie / Sharma, Kumar / Satriano, Joseph

Nephron. Experimental nephrology

2014

Abstract: Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP- ... ...

Abstract	Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion. © 2014 S. Karger AG, Basel.
Language	English
Publishing date	2014-12-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000368932
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Article ; Online: Induction of AMPK activity corrects early pathophysiological alterations in the subtotal nephrectomy model of chronic kidney disease.

Satriano, Joseph / Sharma, Kumar / Blantz, Roland C / Deng, Aihua

American journal of physiology. Renal physiology

2013 Volume 305, Issue 5, Page(s) F727–33

Abstract: The rat kidney ablation and infarction (A/I) model of subtotal or 5/6th nephrectomy is the most commonly studied model of nondiabetic chronic kidney disease (CKD). The A/I kidney at 1 wk exhibits reductions in kidney function, as determined by glomerular ...

Abstract	The rat kidney ablation and infarction (A/I) model of subtotal or 5/6th nephrectomy is the most commonly studied model of nondiabetic chronic kidney disease (CKD). The A/I kidney at 1 wk exhibits reductions in kidney function, as determined by glomerular filtration rate, and diminished metabolic efficiency as determined by oxygen consumption per sodium transport (QO2/TNa). As renoprotective AMPK activity is affected by metabolic changes and cellular stress, we evaluated AMPK activity in this model system. We show that these early pathophysiological changes are accompanied by a paradoxical decrease in AMPK activity. Over time, these kidney parameters progressively worsen with extensive kidney structural, functional, metabolic, and fibrotic changes observed at 4 wk after A/I. We show that induction of AMPK activity with either metformin or 5-aminoimidazole-4-carboxamide ribonucleotide increases AMPK activity in this model and also corrects kidney metabolic inefficiency, improves kidney function, and ameliorates kidney fibrosis and structural alterations. We conclude that AMPK activity is reduced in the subtotal nephrectomy model of nondiabetic CKD, that altered regulation of AMPK is coincident with the progression of disease parameters, and that restoration of AMPK activity can suppress the progressive loss of function characteristic of this model. We propose that induction of AMPK activity may prove an effective therapeutic target for the treatment of nondiabetic CKD.
MeSH term(s)	Adenylate Kinase/biosynthesis ; Animals ; Disease Models, Animal ; Enzyme Induction ; Male ; Metformin/pharmacology ; Nephrectomy ; Rats ; Rats, Wistar ; Renal Insufficiency, Chronic/physiopathology
Chemical Substances	Metformin (9100L32L2N) ; Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2013-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00293.2013
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Article: Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers

Declèves, Anne-Emilie / Sharma, Kumar / Satriano, Joseph

Nephron Experimental Nephrology

2014 Volume 128, Issue 3-4, Page(s) 98–110

Institution	Division of Nephrology-Hypertension, O'Brien Kidney Center Center for Renal Translational Medicine Institute of Metabolomic Medicine Stein Institute for Research on Aging University of California San Diego and the Veterans Affairs San Diego Healthcare System, La Jolla, Calif., USA Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles (ULB), Brussels, Belgium
Abstract	Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion.
Keywords	Mammalian target of rapamycin ; PTEN-induced putative kinase-1 ; p62/SQSTM1 ; Mitophagy
Language	English
Publishing date	2014-12-06
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Original Paper
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000368932
Database	Karger publisher's database

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Article ; Online: Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers

Declèves, Anne-Emilie / Sharma, Kumar / Satriano, Joseph

Nephron Experimental Nephrology

2014 Volume 128, Issue 3-4, Page(s) 110–198

Abstract	Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion.© 2014 S. Karger AG, Basel
Keywords	Mammalian target of rapamycin ; Mitophagy ; p62/SQSTM1 ; PTEN-induced putative kinase-1
Language	English
Publisher	S. Karger AG
Publishing place	Basel
Publishing country	Switzerland
Document type	Article ; Online
ZDB-ID	207121-6
ISSN	1660-2129 ; 1423-0186 ; 0028-2766 ; 0028-2766
ISSN (online)	1660-2129 ; 1423-0186
ISSN	0028-2766
DOI	10.1159/000368932
Database	Karger publisher's database

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Article ; Online: Interactions between HIF-1α and AMPK in the regulation of cellular hypoxia adaptation in chronic kidney disease.

Li, Hui / Satriano, Joseph / Thomas, Joanna L / Miyamoto, Satoshi / Sharma, Kumar / Pastor-Soler, Núria M / Hallows, Kenneth R / Singh, Prabhleen

American journal of physiology. Renal physiology

2015 Volume 309, Issue 5, Page(s) F414–28

Abstract: Renal hypoxia contributes to chronic kidney disease (CKD) progression, as validated in experimental and human CKD. In the early stages, increased oxygen consumption causes oxygen demand/supply mismatch, leading to hypoxia. Hence, early targeting of the ... ...

Abstract	Renal hypoxia contributes to chronic kidney disease (CKD) progression, as validated in experimental and human CKD. In the early stages, increased oxygen consumption causes oxygen demand/supply mismatch, leading to hypoxia. Hence, early targeting of the determinants and regulators of oxygen consumption in CKD may alter the disease course before permanent damage ensues. Here, we focus on hypoxia inducible factor-1α (HIF-1α) and AMP-activated protein kinase (AMPK) and on the mechanisms by which they may facilitate cellular hypoxia adaptation. We found that HIF-1α activation in the subtotal nephrectomy (STN) model of CKD limits protein synthesis, inhibits apoptosis, and activates autophagy, presumably for improved cell survival. AMPK activation was diminished in the STN kidney and was remarkably restored by HIF-1α activation, demonstrating a novel role for HIF-1α in the regulation of AMPK activity. We also investigated the independent and combined effects of HIF-1α and AMPK on cell survival and death pathways by utilizing pharmacological and knockdown approaches in cell culture models. We found that the effect of HIF-1α activation on autophagy is independent of AMPK, but on apoptosis it is partially AMPK dependent. The effects of HIF-1α and AMPK activation on inhibiting protein synthesis via the mTOR pathway appear to be additive. These various effects were also observed under hypoxic conditions. In conclusion, HIF-1α and AMPK appear to be linked at a molecular level and may act as components of a concerted cellular response to hypoxic stress in the pathophysiology of CKD.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adaptation, Physiological/physiology ; Animals ; Apoptosis/physiology ; Autophagy/physiology ; Cell Hypoxia/physiology ; Disease Models, Animal ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Male ; Nephrectomy ; Rats ; Rats, Wistar ; Renal Circulation/physiology ; Renal Insufficiency, Chronic/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, rat (EC 2.7.1.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2015-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00463.2014
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Article: Agmatine effects on mitochondrial membrane potential andNF-κB activation protect against rotenone-induced cell damage in human neuronal-like SH-SY5Y cells

Condello, Salvatore / Currò, Monica / Ferlazzo, Nadia / Caccamo, Daniela / Satriano, Joseph / Ientile, Riccardo

Journal of neurochemistry. 2011 Jan., v. 116, no. 1

2011

Abstract: J. Neurochem. (2011) 116, 67-75. ABSTRACT: Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in the CNS in several models of cellular damage. However, the mechanisms involved in these ... ...

Abstract	J. Neurochem. (2011) 116, 67-75. ABSTRACT: Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in the CNS in several models of cellular damage. However, the mechanisms involved in these protective effects in neurodegenerative diseases are poorly understood. The present study was undertaken to investigate the effects of agmatine on cell injury induced by rotenone, commonly used in establishing in vivo and in vitro models of Parkinson's disease, in human-derived dopaminergic neuroblastoma cell line (SH-SY5Y). We report that agmatine dose-dependently suppressed rotenone-induced cellular injury through a reduction of oxidative stress. Similar effects were obtained by spermine, suggesting a scavenging effect for these compounds. However, unlike spermine, agmatine also prevented rotenone-induced nuclear factor-κB nuclear translocation and mitochondrial membrane potential dissipation. Furthermore, rotenone-induced increase in apoptotic markers, such as caspase 3 activity, Bax expression and cytochrome c release, was significantly attenuated with agmatine treatment. These findings demonstrate mitochondrial preservation with agmatine in a rotenone model of apoptotic cell death, and that the neuroprotective action of agmatine appears because of suppressing apoptotic signalling mechanisms. Thus, agmatine may have therapeutic potential in the treatment of Parkinson's disease by protecting dopaminergic neurons.
Language	English
Dates of publication	2011-01
Size	p. 67-75.
Publishing place	Blackwell Publishing Ltd
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.07085.x
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Agmatine effects on mitochondrial membrane potential and NF-κB activation protect against rotenone-induced cell damage in human neuronal-like SH-SY5Y cells.

Condello, Salvatore / Currò, Monica / Ferlazzo, Nadia / Caccamo, Daniela / Satriano, Joseph / Ientile, Riccardo

Journal of neurochemistry

2011 Volume 116, Issue 1, Page(s) 67–75

Abstract: Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in the CNS in several models of cellular damage. However, the mechanisms involved in these protective effects in neurodegenerative ... ...

Abstract	Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in the CNS in several models of cellular damage. However, the mechanisms involved in these protective effects in neurodegenerative diseases are poorly understood. The present study was undertaken to investigate the effects of agmatine on cell injury induced by rotenone, commonly used in establishing in vivo and in vitro models of Parkinson's disease, in human-derived dopaminergic neuroblastoma cell line (SH-SY5Y). We report that agmatine dose-dependently suppressed rotenone-induced cellular injury through a reduction of oxidative stress. Similar effects were obtained by spermine, suggesting a scavenging effect for these compounds. However, unlike spermine, agmatine also prevented rotenone-induced nuclear factor-κB nuclear translocation and mitochondrial membrane potential dissipation. Furthermore, rotenone-induced increase in apoptotic markers, such as caspase 3 activity, Bax expression and cytochrome c release, was significantly attenuated with agmatine treatment. These findings demonstrate mitochondrial preservation with agmatine in a rotenone model of apoptotic cell death, and that the neuroprotective action of agmatine appears because of suppressing apoptotic signalling mechanisms. Thus, agmatine may have therapeutic potential in the treatment of Parkinson's disease by protecting dopaminergic neurons.
MeSH term(s)	Agmatine/pharmacology ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Death/drug effects ; Cell Death/physiology ; Cell Line, Tumor ; Humans ; Membrane Potential, Mitochondrial/drug effects ; Membrane Potential, Mitochondrial/physiology ; NF-kappa B/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotective Agents/pharmacology ; Rotenone/toxicity
Chemical Substances	NF-kappa B ; Neuroprotective Agents ; Rotenone (03L9OT429T) ; Agmatine (70J407ZL5Q)
Language	English
Publishing date	2011-01
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.07085.x
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Article ; Online: SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice.

Vallon, Volker / Gerasimova, Maria / Rose, Michael A / Masuda, Takahiro / Satriano, Joseph / Mayoux, Eric / Koepsell, Hermann / Thomson, Scott C / Rieg, Timo

American journal of physiology. Renal physiology

2013 Volume 306, Issue 2, Page(s) F194–204

Abstract: Our previous work has shown that gene knockout of the sodium-glucose cotransporter SGLT2 modestly lowered blood glucose in streptozotocin-diabetic mice (BG; from 470 to 300 mg/dl) and prevented glomerular hyperfiltration but did not attenuate albuminuria ...

Abstract	Our previous work has shown that gene knockout of the sodium-glucose cotransporter SGLT2 modestly lowered blood glucose in streptozotocin-diabetic mice (BG; from 470 to 300 mg/dl) and prevented glomerular hyperfiltration but did not attenuate albuminuria or renal growth and inflammation. Here we determined effects of the SGLT2 inhibitor empagliflozin (300 mg/kg of diet for 15 wk; corresponding to 60-80 mg·kg(-1)·day(-1)) in type 1 diabetic Akita mice that, opposite to streptozotocin-diabetes, upregulate renal SGLT2 expression. Akita diabetes, empagliflozin, and Akita + empagliflozin similarly increased renal membrane SGLT2 expression (by 38-56%) and reduced the expression of SGLT1 (by 33-37%) vs. vehicle-treated wild-type controls (WT). The diabetes-induced changes in SGLT2/SGLT1 protein expression are expected to enhance the BG-lowering potential of SGLT2 inhibition, and empagliflozin strongly lowered BG in Akita (means of 187-237 vs. 517-535 mg/dl in vehicle group; 100-140 mg/dl in WT). Empagliflozin modestly reduced GFR in WT (250 vs. 306 μl/min) and completely prevented the diabetes-induced increase in glomerular filtration rate (GFR) (255 vs. 397 μl/min). Empagliflozin attenuated increases in kidney weight and urinary albumin/creatinine ratio in Akita in proportion to hyperglycemia. Empagliflozin did not increase urinary glucose/creatinine ratios in Akita, indicating the reduction in filtered glucose balanced the inhibition of glucose reabsorption. Empagliflozin attenuated/prevented the increase in systolic blood pressure, glomerular size, and molecular markers of kidney growth, inflammation, and gluconeogenesis in Akita. We propose that SGLT2 inhibition can lower GFR independent of reducing BG (consistent with the tubular hypothesis of diabetic glomerular hyperfiltration), while attenuation of albuminuria, kidney growth, and inflammation in the early diabetic kidney may mostly be secondary to lower BG.
MeSH term(s)	Adipocytes/drug effects ; Adipocytes/ultrastructure ; Albuminuria/drug therapy ; Animals ; Benzhydryl Compounds/pharmacology ; Biomarkers/metabolism ; Blood Glucose/metabolism ; Blood Pressure/physiology ; Blotting, Western ; Diabetes Mellitus/genetics ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/prevention & control ; Drinking/physiology ; Eating/physiology ; Glomerular Filtration Rate/drug effects ; Glucosides/pharmacology ; Heart Rate/physiology ; Hyperglycemia/complications ; Hyperglycemia/metabolism ; Inflammation/metabolism ; Kidney/drug effects ; Kidney/growth & development ; Kidney/pathology ; Kidney Glomerulus/growth & development ; Kidney Glomerulus/metabolism ; Mice ; Mice, Inbred Strains ; Real-Time Polymerase Chain Reaction ; Sodium-Glucose Transporter 1/biosynthesis ; Sodium-Glucose Transporter 1/genetics ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors
Chemical Substances	Benzhydryl Compounds ; Biomarkers ; Blood Glucose ; Glucosides ; Slc5a1 protein, mouse ; Slc5a2 protein, mouse ; Sodium-Glucose Transporter 1 ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors ; empagliflozin (HDC1R2M35U)
Language	English
Publishing date	2013-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00520.2013
Database	MEDical Literature Analysis and Retrieval System OnLINE

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