LIVIVO - Search results -

Search results

Result 1 - 10 of total 21

Search options

Article ; Online: Recent Developments in Heart Failure.

Dassanayaka, Sujith / Jones, Steven P

2015 Volume 117, Issue 7, Page(s) e58–63

MeSH term(s)	Animals ; Genetic Therapy/trends ; Heart Failure/diagnosis ; Heart Failure/genetics ; Heart Failure/therapy ; Humans ; Stem Cell Transplantation/trends ; Ventricular Remodeling/genetics
Language	English
Publishing date	2015-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.115.305765
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: O-GlcNAc and the cardiovascular system.

Dassanayaka, Sujith / Jones, Steven P

Pharmacology & therapeutics

2013 Volume 142, Issue 1, Page(s) 62–71

Abstract: The cardiovascular system is capable of robust changes in response to physiologic and pathologic stimuli through intricate signaling mechanisms. The area of metabolism has witnessed a veritable renaissance in the cardiovascular system. In particular, the ...

Abstract	The cardiovascular system is capable of robust changes in response to physiologic and pathologic stimuli through intricate signaling mechanisms. The area of metabolism has witnessed a veritable renaissance in the cardiovascular system. In particular, the post-translational β-O-linkage of N-acetylglucosamine (O-GlcNAc) to cellular proteins represents one such signaling pathway that has been implicated in the pathophysiology of cardiovascular disease. This highly dynamic protein modification may induce functional changes in proteins and regulate key cellular processes including translation, transcription, and cell death. In addition, its potential interplay with phosphorylation provides an additional layer of complexity to post-translational regulation. The hexosamine biosynthetic pathway generally requires glucose to form the nucleotide sugar, UDP-GlcNAc. Accordingly, O-GlcNAcylation may be altered in response to nutrient availability and cellular stress. Recent literature supports O-GlcNAcylation as an autoprotective response in models of acute stress (hypoxia, ischemia, oxidative stress). Models of sustained stress, such as pressure overload hypertrophy, and infarct-induced heart failure, may also require protein O-GlcNAcylation as a partial compensatory mechanism. Yet, in models of Type II diabetes, O-GlcNAcylation has been implicated in the subsequent development of vascular, and even cardiac, dysfunction. This review will address this apparent paradox and discuss the potential mechanisms of O-GlcNAc-mediated cardioprotection and cardiovascular dysfunction. This discussion will also address potential targets for pharmacologic interventions and the unique considerations related to such targets.
MeSH term(s)	Acetylglucosamine/metabolism ; Animals ; Cardiovascular System/metabolism ; Exercise ; Hexosamines/metabolism ; Humans ; Protein Processing, Post-Translational
Chemical Substances	Hexosamines ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2013-11-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2013.11.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1183: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.

Zelko, Igor N / Dassanayaka, Sujith / Malovichko, Marina V / Howard, Caitlin M / Garrett, Lauren F / Uchida, Shizuka / Brittian, Kenneth R / Conklin, Daniel J / Jones, Steven P / Srivastava, Sanjay

Toxicological sciences : an official journal of the Society of Toxicology

2021 Volume 185, Issue 1, Page(s) 64–76

Abstract: Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals, and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of ... ...

Abstract	Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals, and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, and 6 weeks) or high-efficiency particulate absorbing-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone, and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5- to 2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.
MeSH term(s)	Animals ; Benzene/toxicity ; Endothelial Cells/metabolism ; Heart Failure ; Male ; Mice ; Mice, Inbred C57BL ; Ventricular Remodeling/physiology
Chemical Substances	Benzene (J64922108F)
Language	English
Publishing date	2021-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfab125
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1709: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Mechanistic pathway(s) of acquired von willebrand syndrome with a continuous-flow ventricular assist device: in vitro findings.

Dassanayaka, Sujith / Slaughter, Mark S / Bartoli, Carlo R

ASAIO journal (American Society for Artificial Internal Organs : 1992)

2013 Volume 59, Issue 2, Page(s) 123–129

Abstract: In patients with a ventricular assist device (VAD), diminished high-molecular-weight von Willebrand factor (vWF) multimers may contribute to a bleeding diathesis. The mechanistic pathway(s) of vWF degradation and the role of ADAMTS-13, the vWF-cleaving ... ...

Abstract	In patients with a ventricular assist device (VAD), diminished high-molecular-weight von Willebrand factor (vWF) multimers may contribute to a bleeding diathesis. The mechanistic pathway(s) of vWF degradation and the role of ADAMTS-13, the vWF-cleaving metalloproteinase, are unknown. The objective of this study was to investigate the molecular mechanisms of VAD-induced vWF impairment in an in vitro system.Simple, mock circulatory loops (n = 4) were developed with a clinically approved, paracorporeal continuous-flow VAD. The loops were primed with anticoagulated, whole bovine blood (750 ml). The VAD was operated at constant blood flow and pressure. Blood samples were drawn at baseline and hourly for 6 hours. vWF multimers and ADAMTS-13 protein were quantified by agarose and polyacrylamide gel electrophoresis with immunoblotting. Plasma platelet factor 4 (PF4), a marker of platelet activation, was quantified via ELISA.Within 120 minutes, high-molecular-weight vWF multimers decreased, and low-molecular-weight multimers increased. Multiple low-molecular-weight vWF fragments emerged (~140, 176, 225, and 310 kDa). Total plasma ADAMTS-13 increased by 13 ± 3% (p < 0.05). Plasma PF4 increased by 21 ± 7% (p = 0.05).During VAD support, vWF degradation occurred quickly. Multiple mechanisms were responsible and included vWF cleavage by ADAMTS-13 (140 and 176 kDa fragments), and what may have been mechanical demolition of endogenous plasma vWF (225 kDa fragments) and nascent vWF (225 and 310 kDa fragments) from platelets. A modest increase in plasma ADAMTS-13 from activated platelets may have contributed to this process but was not the major mechanism. Mechanical demolition was likely the dominant process and warrants further evaluation.
MeSH term(s)	ADAM Proteins/blood ; ADAM Proteins/physiology ; ADAMTS13 Protein ; Animals ; Cattle ; Heart-Assist Devices ; Molecular Weight ; Platelet Factor 4/blood ; Shear Strength ; von Willebrand Diseases/blood ; von Willebrand Diseases/surgery ; von Willebrand Factor/metabolism
Chemical Substances	von Willebrand Factor ; Platelet Factor 4 (37270-94-3) ; ADAM Proteins (EC 3.4.24.-) ; ADAMTS13 Protein (EC 3.4.24.87) ; ADAMTS13 protein, human (EC 3.4.24.87)
Language	English
Publishing date	2013-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	759982-1
ISSN	1538-943X ; 0162-1432 ; 1058-2916
ISSN (online)	1538-943X
ISSN	0162-1432 ; 1058-2916
DOI	10.1097/MAT.0b013e318283815c
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uk I Zs.199: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.B 2435: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overload.

Audam, Timothy N / Howard, Caitlin M / Garrett, Lauren F / Zheng, Yi Wei / Bradley, James A / Brittian, Kenneth R / Frank, Matthew W / Fulghum, Kyle L / Pólos, Miklós / Herczeg, Szilvia / Merkely, Béla / Radovits, Tamás / Uchida, Shizuka / Hill, Bradford G / Dassanayaka, Sujith / Jackowski, Suzanne / Jones, Steven P

American journal of physiology. Heart and circulatory physiology

2021 Volume 321, Issue 4, Page(s) H784–H797

Abstract: Coenzyme A (CoA) is an essential cofactor required for intermediary metabolism. Perturbations in homeostasis of CoA have been implicated in various pathologies; however, whether CoA homeostasis is changed and the extent to which CoA levels contribute to ... ...

Abstract	Coenzyme A (CoA) is an essential cofactor required for intermediary metabolism. Perturbations in homeostasis of CoA have been implicated in various pathologies; however, whether CoA homeostasis is changed and the extent to which CoA levels contribute to ventricular function and remodeling during pressure overload has not been explored. In this study, we sought to assess changes in CoA biosynthetic pathway during pressure overload and determine the impact of limiting CoA on cardiac function. We limited cardiac CoA levels by deleting the rate-limiting enzyme in CoA biosynthesis, pantothenate kinase 1 (
MeSH term(s)	Animals ; Aorta/physiopathology ; Aorta/surgery ; Apoptosis ; Arterial Pressure ; Coenzyme A/metabolism ; Disease Models, Animal ; Energy Metabolism ; Female ; Fibrosis ; Gene Deletion ; Humans ; Male ; Metabolome ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/enzymology ; Myocardium/pathology ; Phosphotransferases (Alcohol Group Acceptor)/deficiency ; Phosphotransferases (Alcohol Group Acceptor)/genetics ; Transcriptome ; Ventricular Dysfunction, Left/enzymology ; Ventricular Dysfunction, Left/genetics ; Ventricular Dysfunction, Left/pathology ; Ventricular Dysfunction, Left/physiopathology ; Ventricular Function, Left ; Ventricular Remodeling ; Mice
Chemical Substances	Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; pantothenate kinase (EC 2.7.1.33) ; Coenzyme A (SAA04E81UX)
Language	English
Publishing date	2021-09-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00411.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: E2F1 Transcription Factor Regulates O-linked N-acetylglucosamine (O-GlcNAc) Transferase and O-GlcNAcase Expression.

Muthusamy, Senthilkumar / Hong, Kyung U / Dassanayaka, Sujith / Hamid, Tariq / Jones, Steven P

The Journal of biological chemistry

2015 Volume 290, Issue 52, Page(s) 31013–31024

Abstract: Protein O-GlcNAcylation, which is controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), has emerged as an important posttranslational modification that may factor in multiple diseases. Until recently, it was assumed that OGT/OGA protein ... ...

Abstract	Protein O-GlcNAcylation, which is controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), has emerged as an important posttranslational modification that may factor in multiple diseases. Until recently, it was assumed that OGT/OGA protein expression was relatively constant. Several groups, including ours, have shown that OGT and/or OGA expression changes in several pathologic contexts, yet the cis and trans elements that regulate the expression of these enzymes remain essentially unexplored. Here, we used a reporter-based assay to analyze minimal promoters and leveraged in silico modeling to nominate several candidate transcription factor binding sites in both Ogt (i.e. the gene for OGT protein) and Mgea5 (i.e. the gene for OGA protein). We noted multiple E2F binding site consensus sequences in both promoters. We performed chromatin immunoprecipitation in both human and mouse cells and found that E2F1 bound to candidate E2F binding sites in both promoters. In HEK293 cells, we overexpressed E2F1, which significantly reduced OGT and MGEA5 expression. Conversely, E2F1-deficient mouse fibroblasts had increased Ogt and Mgea5 expression. Of the known binding partners for E2F1, we queried whether retinoblastoma 1 (Rb1) might be involved. Rb1-deficient mouse embryonic fibroblasts showed increased levels of Ogt and Mgea5 expression, yet overexpression of E2F1 in the Rb1-deficient cells did not alter Ogt and Mgea5 expression, suggesting that Rb1 is required for E2F1-mediated suppression. In conclusion, this work identifies and validates some of the promoter elements for mouse Ogt and Mgea5 genes. Specifically, E2F1 negatively regulates both Ogt and Mgea5 expression in an Rb1 protein-dependent manner.
MeSH term(s)	3T3-L1 Cells ; Animals ; Antigens, Neoplasm/biosynthesis ; Antigens, Neoplasm/genetics ; E2F1 Transcription Factor/genetics ; E2F1 Transcription Factor/metabolism ; Gene Expression Regulation, Enzymologic/physiology ; HEK293 Cells ; Histone Acetyltransferases/biosynthesis ; Histone Acetyltransferases/genetics ; Humans ; Hyaluronoglucosaminidase/biosynthesis ; Hyaluronoglucosaminidase/genetics ; Mice ; Mice, Mutant Strains ; N-Acetylglucosaminyltransferases/biosynthesis ; N-Acetylglucosaminyltransferases/genetics ; Response Elements/physiology ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism
Chemical Substances	Antigens, Neoplasm ; E2F1 Transcription Factor ; E2F1 protein, human ; E2f1 protein, mouse ; Retinoblastoma Protein ; Histone Acetyltransferases (EC 2.3.1.48) ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; UDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase (EC 2.4.1.-) ; OGA protein, human (EC 3.2.1.169) ; Hyaluronoglucosaminidase (EC 3.2.1.35)
Language	English
Publishing date	2015-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M115.677534
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.108: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cardiomyocyte Oga haploinsufficiency increases O-GlcNAcylation but hastens ventricular dysfunction following myocardial infarction.

Dassanayaka, Sujith / Brittian, Kenneth R / Long, Bethany W / Higgins, Lauren A / Bradley, James A / Audam, Timothy N / Jurkovic, Andrea / Gumpert, Anna M / Harrison, Linda T / Hartyánszky, István / Perge, Péter / Merkely, Béla / Radovits, Tamás / Hanover, John A / Jones, Steven P

PloS one

2020 Volume 15, Issue 11, Page(s) e0242250

Abstract: Rationale: The beta-O-linkage of N-acetylglucosamine (i.e., O-GlcNAc) to proteins is a pro-adaptive response to cellular insults. To this end, increased protein O-GlcNAcylation improves short-term survival of cardiomyocytes subjected to acute injury. ... ...

Abstract	Rationale: The beta-O-linkage of N-acetylglucosamine (i.e., O-GlcNAc) to proteins is a pro-adaptive response to cellular insults. To this end, increased protein O-GlcNAcylation improves short-term survival of cardiomyocytes subjected to acute injury. This observation has been repeated by multiple groups and in multiple models; however, whether increased protein O-GlcNAcylation plays a beneficial role in more chronic settings remains an open question. Objective: Here, we queried whether increasing levels of cardiac protein O-GlcNAcylation would be beneficial during infarct-induced heart failure. Methods and results: To achieve increased protein O-GlcNAcylation, we targeted Oga, the gene responsible for removing O-GlcNAc from proteins. Here, we generated mice with cardiomyocyte-restricted, tamoxifen-inducible haploinsufficient Oga gene. In the absence of infarction, we observed a slight reduction in ejection fraction in Oga deficient mice. Overall, Oga reduction had no major impact on ventricular function. In additional cohorts, mice of both sexes and both genotypes were subjected to infarct-induced heart failure and followed for up to four weeks, during which time cardiac function was assessed via echocardiography. Contrary to our prediction, the Oga deficient mice exhibited exacerbated-not improved-cardiac function at one week following infarction. When the observation was extended to 4 wk post-MI, this acute exacerbation was lost. Conclusions: The present findings, coupled with our previous work, suggest that altering the ability of cardiomyocytes to either add or remove O-GlcNAc modifications to proteins exacerbates early infarct-induced heart failure. We speculate that more nuanced approaches to regulating O-GlcNAcylation are needed to understand its role-and, in particular, the possibility of cycling, in the pathophysiology of the failing heart.
MeSH term(s)	Animals ; Echocardiography ; Female ; Glycosylation ; Haploinsufficiency ; Heart/physiology ; Heart Failure/metabolism ; Heart Failure/pathology ; Humans ; Male ; Mice ; Mice, Knockout ; Middle Aged ; Myocardial Infarction/complications ; Myocardial Infarction/pathology ; Myocardium/enzymology ; Myocardium/metabolism ; Myocardium/pathology ; N-Acetylglucosaminyltransferases/deficiency ; N-Acetylglucosaminyltransferases/genetics ; N-Acetylglucosaminyltransferases/metabolism ; Tamoxifen/pharmacology ; Up-Regulation ; Ventricular Dysfunction/etiology ; Ventricular Function/drug effects
Chemical Substances	Tamoxifen (094ZI81Y45) ; N-Acetylglucosaminyltransferases (EC 2.4.1.-)
Language	English
Publishing date	2020-11-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0242250
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Airn

Hosen, Mohammed Rabiul / Militello, Giuseppe / Weirick, Tyler / Ponomareva, Yuliya / Dassanayaka, Sujith / Moore, Joseph B / Döring, Claudia / Wysoczynski, Marcin / Jones, Steven P / Dimmeler, Stefanie / Uchida, Shizuka

Circulation research

2018 Volume 122, Issue 10, Page(s) 1347–1353

Abstract: Rationale: Increasing evidence indicates the presence of lncRNAs in various cell types. : Objective: Here, we studied the functions of : Methods and results: Silencing of : Conclusions: Our study uncovers a new function ... ...

Abstract	Rationale: Increasing evidence indicates the presence of lncRNAs in various cell types. Objective: Here, we studied the functions of Methods and results: Silencing of Conclusions: Our study uncovers a new function of
MeSH term(s)	Animals ; Cell Line ; Cell Movement ; Gene Expression Regulation ; Mice ; Myocardial Infarction/metabolism ; Myocytes, Cardiac/metabolism ; Organ Specificity ; Protein Binding ; Protein Biosynthesis ; RNA Interference ; RNA Splicing ; RNA, Long Noncoding/genetics ; RNA, Messenger/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; RNA-Binding Proteins/biosynthesis ; RNA-Binding Proteins/genetics ; Replication Protein A/metabolism
Chemical Substances	Air non-coding RNA, mouse ; IGF2BP2 protein, mouse ; RNA, Long Noncoding ; RNA, Messenger ; RNA, Small Interfering ; RNA-Binding Proteins ; Replication Protein A ; Rpa1 protein, mouse
Language	English
Publishing date	2018-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.117.312215
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cardiac-specific overexpression of aldehyde dehydrogenase 2 exacerbates cardiac remodeling in response to pressure overload.

Dassanayaka, Sujith / Zheng, Yuting / Gibb, Andrew A / Cummins, Timothy D / McNally, Lindsey A / Brittian, Kenneth R / Jagatheesan, Ganapathy / Audam, Timothy N / Long, Bethany W / Brainard, Robert E / Jones, Steven P / Hill, Bradford G

Redox biology

2018 Volume 17, Page(s) 440–449

Abstract: Pathological cardiac remodeling during heart failure is associated with higher levels of lipid peroxidation products and lower abundance of several aldehyde detoxification enzymes, including aldehyde dehydrogenase 2 (ALDH2). An emerging idea that could ... ...

Abstract	Pathological cardiac remodeling during heart failure is associated with higher levels of lipid peroxidation products and lower abundance of several aldehyde detoxification enzymes, including aldehyde dehydrogenase 2 (ALDH2). An emerging idea that could explain these findings concerns the role of electrophilic species in redox signaling, which may be important for adaptive responses to stress or injury. The purpose of this study was to determine whether genetically increasing ALDH2 activity affects pressure overload-induced cardiac dysfunction. Mice subjected to transverse aortic constriction (TAC) for 12 weeks developed myocardial hypertrophy and cardiac dysfunction, which were associated with diminished ALDH2 expression and activity. Cardiac-specific expression of the human ALDH2 gene in mice augmented myocardial ALDH2 activity but did not improve cardiac function in response to pressure overload. After 12 weeks of TAC, ALDH2 transgenic mice had larger hearts than their wild-type littermates and lower capillary density. These findings show that overexpression of ALDH2 augments the hypertrophic response to pressure overload and imply that downregulation of ALDH2 may be an adaptive response to certain forms of cardiac pathology.
MeSH term(s)	Aldehyde Dehydrogenase, Mitochondrial/genetics ; Animals ; Aorta/metabolism ; Gene Expression Regulation ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Failure/pathology ; Humans ; Mice ; Mice, Transgenic ; Mitochondria/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Oxidation-Reduction ; Oxidative Stress/genetics ; Pressure ; Signal Transduction/genetics ; Ventricular Remodeling/genetics
Chemical Substances	ALDH2 protein, human (EC 1.2.1.3) ; Aldehyde Dehydrogenase, Mitochondrial (EC 1.2.1.3)
Language	English
Publishing date	2018-06-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2018.05.016
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Deficiency of aldose reductase exacerbates early pressure overload-induced cardiac dysfunction and autophagy in mice.

Baba, Shahid P / Zhang, Deqing / Singh, Mahavir / Dassanayaka, Sujith / Xie, Zhengzhi / Jagatheesan, Ganapathy / Zhao, Jingjing / Schmidtke, Virginia K / Brittian, Kenneth R / Merchant, Michael L / Conklin, Daniel J / Jones, Steven P / Bhatnagar, Aruni

Journal of molecular and cellular cardiology

2018 Volume 118, Page(s) 183–192

Abstract: Pathological cardiac hypertrophy is associated with the accumulation of lipid peroxidation-derived aldehydes such as 4-hydroxy-trans-2-nonenal (HNE) and acrolein in the heart. These aldehydes are metabolized via several pathways, of which aldose ... ...

Abstract	Pathological cardiac hypertrophy is associated with the accumulation of lipid peroxidation-derived aldehydes such as 4-hydroxy-trans-2-nonenal (HNE) and acrolein in the heart. These aldehydes are metabolized via several pathways, of which aldose reductase (AR) represents a broad-specificity route for their elimination. We tested the hypothesis that by preventing aldehyde removal, AR deficiency accentuates the pathological effects of transverse aortic constriction (TAC). We found that the levels of AR in the heart were increased in mice subjected to TAC for 2 weeks. In comparison with wild-type (WT), AR-null mice showed lower ejection fraction, which was exacerbated 2 weeks after TAC. Levels of atrial natriuretic peptide and myosin heavy chain were higher in AR-null than in WT TAC hearts. Deficiency of AR decreased urinary levels of the acrolein metabolite, 3-hydroxypropylmercapturic acid. Deletion of AR did not affect the levels of the other aldehyde-metabolizing enzyme - aldehyde dehydrogenase 2 in the heart, or its urinary product - (N-Acetyl-S-(2-carboxyethyl)-l-cystiene). AR-null hearts subjected to TAC showed increased accumulation of HNE- and acrolein-modified proteins, as well as increased AMPK phosphorylation and autophagy. Superfusion with HNE led to a greater increase in p62, LC3II formation, and GFP-LC3-II punctae formation in AR-null than WT cardiac myocytes. Pharmacological inactivation of JNK decreased HNE-induced autophagy in AR-null cardiac myocytes. Collectively, these results suggest that during hypertrophy the accumulation of lipid peroxidation derived aldehydes promotes pathological remodeling via excessive autophagy, and that metabolic detoxification of these aldehydes by AR may be essential for maintaining cardiac function during early stages of pressure overload.
MeSH term(s)	Aldehyde Reductase/deficiency ; Aldehyde Reductase/metabolism ; Aldehydes/metabolism ; Animals ; Aorta/pathology ; Autophagy ; Cardiomegaly/diagnostic imaging ; Cardiomegaly/enzymology ; Cardiomegaly/pathology ; Cardiomegaly/physiopathology ; Constriction, Pathologic ; Gene Deletion ; Heart/physiopathology ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Mice, Inbred C57BL ; Myocardial Contraction ; Myocardium/enzymology ; Pressure ; Sequestosome-1 Protein/metabolism
Chemical Substances	Aldehydes ; Sequestosome-1 Protein ; Sqstm1 protein, mouse ; Aldehyde Reductase (EC 1.1.1.21) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; 4-hydroxy-2-nonenal (K1CVM13F96)
Language	English
Publishing date	2018-04-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2018.04.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito