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Article ; Online: Myofibroblast modulation of cardiac myocyte structure and function.

Nagaraju, Chandan K / Dries, Eef / Gilbert, Guillaume / Abdesselem, Mouna / Wang, Nan / Amoni, Matthew / Driesen, Ronald B / Sipido, Karin R

Scientific reports

2019 Volume 9, Issue 1, Page(s) 8879

Abstract: After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac ... ...

Abstract	After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac myocytes (CMs) but insight into the phenotype-specific role and mode of interaction is still incomplete. Our objectives are to further define the modulation of CMs by MyoFbs compared to Fbs, as well as the role of direct contact through gap junctions vs. soluble mediators, using Fbs and CMs from pig left ventricle. Fbs were treated to maintain an undifferentiated state (SD-208) or to attain full differentiation to MyoFb (TGF-β1). Fbs and MyoFbs were co-cultured with CMs, with the possibility of direct contact or separated by a Thincert membrane. Only in direct co-culture, both Fbs and MyoFbs were able to decrease CM viability after 2 days. Only MyoFbs induced significant distal spreading of CMs in both direct and indirect co-culture. MyoFbs, but not Fbs, readily made connections with CMs in direct co-culture and connexin 43 expression in MyoFb was higher than in Fb. When coupled to CMs, MyoFbs reduced the CM action potential duration and hyperpolarized the CM resting membrane potential. Uncoupling reversed these effects. In conclusion, MyoFbs, but not Fbs, alter the CM structural phenotype. MyoFbs, but not Fbs, are likely to electrically connect to CMs and thereby modulate the CM membrane potential. These data provide further support for an active role of MyoFbs in the arrhythmogenic substrate after cardiac remodelling.
MeSH term(s)	Animals ; Cell Differentiation ; Coculture Techniques ; Membranes, Artificial ; Myocytes, Cardiac/cytology ; Myofibroblasts/cytology ; Swine ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Membranes, Artificial ; Transforming Growth Factor beta1
Language	English
Publishing date	2019-06-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-45078-2
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Article ; Online: MSK-Mediated Phosphorylation of Histone H3 Ser28 Couples MAPK Signalling with Early Gene Induction and Cardiac Hypertrophy.

Robinson, Emma L / Drawnel, Faye M / Mehdi, Saher / Archer, Caroline R / Liu, Wei / Okkenhaug, Hanneke / Alkass, Kanar / Aronsen, Jan Magnus / Nagaraju, Chandan K / Sjaastad, Ivar / Sipido, Karin R / Bergmann, Olaf / Arthur, J Simon C / Wang, Xin / Roderick, H Llewelyn

Cells

2022 Volume 11, Issue 4

Abstract: Heart failure is a leading cause of death that develops subsequent to deleterious hypertrophic cardiac remodelling. MAPK pathways play a key role in coordinating the induction of gene expression during hypertrophy. Induction of the immediate early gene ( ... ...

Abstract	Heart failure is a leading cause of death that develops subsequent to deleterious hypertrophic cardiac remodelling. MAPK pathways play a key role in coordinating the induction of gene expression during hypertrophy. Induction of the immediate early gene (IEG) response including activator protein 1 (AP-1) complex factors is a necessary and early event in this process. How MAPK and IEG expression are coupled during cardiac hypertrophy is not resolved. Here, in vitro, in rodent models and in human samples, we demonstrate that MAPK-stimulated IEG induction depends on the mitogen and stress-activated protein kinase (MSK) and its phosphorylation of histone H3 at serine 28 (pH3S28). pH3S28 in IEG promoters in turn recruits Brg1, a BAF60 ATP-dependent chromatin remodelling complex component, initiating gene expression. Without MSK activity and IEG induction, the hypertrophic response is suppressed. These studies provide new mechanistic insights into the role of MAPK pathways in signalling to the epigenome and regulation of gene expression during cardiac hypertrophy.
MeSH term(s)	Cardiomegaly/genetics ; Chromatin Assembly and Disassembly ; Gene Expression ; Histones/metabolism ; Humans ; Phosphorylation ; Serine/metabolism
Chemical Substances	Histones ; Serine (452VLY9402)
Language	English
Publishing date	2022-02-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11040604
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Article ; Online: InsP

Jin, Xin / Amoni, Matthew / Gilbert, Guillaume / Dries, Eef / Doñate Puertas, Rosa / Tomar, Ashutosh / Nagaraju, Chandan K / Pradhan, Ankit / Yule, David I / Martens, Tobie / Menten, Roxane / Vanden Berghe, Pieter / Rega, Filip / Sipido, Karin / Roderick, H Llewelyn

Basic research in cardiology

2022 Volume 117, Issue 1, Page(s) 60

Abstract: Dysregulated intracellular ... ...

Abstract	Dysregulated intracellular Ca
MeSH term(s)	Humans ; Animals ; Ryanodine Receptor Calcium Release Channel/metabolism ; Calcium/metabolism ; Myocytes, Cardiac/metabolism ; Arrhythmias, Cardiac/metabolism ; Heart Failure/metabolism ; Calcium Signaling
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-11-15
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-022-00967-y
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Article ; Online: Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instability.

Dries, Eef / Amoni, Matthew / Vandenberk, Bert / Johnson, Daniel M / Gilbert, Guillaume / Nagaraju, Chandan K / Puertas, Rosa Doñate / Abdesselem, Mouna / Santiago, Demetrio J / Roderick, H Llewelyn / Claus, Piet / Willems, Rik / Sipido, Karin R

The Journal of physiology

2020 Volume 598, Issue 14, Page(s) 2875–2895

Abstract: Key points: Ventricular arrhythmias are a major complication after myocardial infarction (MI), associated with sympathetic activation. The structurally heterogeneous peri-infarct zone is a known substrate, but the functional role of the myocytes is less ...

Abstract	Key points: Ventricular arrhythmias are a major complication after myocardial infarction (MI), associated with sympathetic activation. The structurally heterogeneous peri-infarct zone is a known substrate, but the functional role of the myocytes is less well known. Recordings of monophasic action potentials in vivo reveal that the peri-infarct zone is a source of delayed afterdepolarizations (DADs) and has a high beat-to-beat variability of repolarization (BVR) during adrenergic stimulation (isoproterenol, ISO). Myocytes isolated from the peri-infarct region have more DADs and spontaneous action potentials, with spontaneous Ca Abstract: Ventricular arrhythmias are a major early complication after myocardial infarction (MI). The heterogeneous peri-infarct zone forms a substrate for re-entry while arrhythmia initiation is often associated with sympathetic activation. We studied the mechanisms triggering these post-MI arrhythmias in vivo and their relation to regional myocyte remodelling. In pigs with chronic MI (6 weeks), in vivo monophasic action potentials were simultaneously recorded in the peri-infarct and remote regions during adrenergic stimulation with isoproterenol (isoprenaline; ISO). Sham animals served as controls. During infusion of ISO in vivo, the incidence of delayed afterdepolarizations (DADs) and beat-to-beat variability of repolarization (BVR) was higher in the peri-infarct than in the remote region. Myocytes isolated from the peri-infarct region, in comparison to myocytes from the remote region, had more DADs, associated with spontaneous Ca
MeSH term(s)	Action Potentials ; Adrenergic Agents ; Animals ; Arrhythmias, Cardiac/etiology ; Myocardial Infarction ; Myocytes, Cardiac ; Swine
Chemical Substances	Adrenergic Agents
Language	English
Publishing date	2020-02-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP278839
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Article ; Online: Myofibroblast Phenotype and Reversibility of Fibrosis in Patients With End-Stage Heart Failure.

Nagaraju, Chandan K / Robinson, Emma L / Abdesselem, Mouna / Trenson, Sander / Dries, Eef / Gilbert, Guillaume / Janssens, Stefan / Van Cleemput, Johan / Rega, Filip / Meyns, Bart / Roderick, H Llewelyn / Driesen, Ronald B / Sipido, Karin R

Journal of the American College of Cardiology

2019 Volume 73, Issue 18, Page(s) 2267–2282

Abstract: Background: Interstitial fibrosis is an important component of diastolic, and systolic, dysfunction in heart failure (HF) and depends on activation and differentiation of fibroblasts into myofibroblasts (MyoFb). Recent clinical evidence suggests that in ...

Abstract	Background: Interstitial fibrosis is an important component of diastolic, and systolic, dysfunction in heart failure (HF) and depends on activation and differentiation of fibroblasts into myofibroblasts (MyoFb). Recent clinical evidence suggests that in late-stage HF, fibrosis is not reversible. Objectives: The study aims to examine the degree of differentiation of cardiac MyoFb in end-stage HF and the potential for their phenotypic reversibility. Methods: Fibroblasts were isolated from the left ventricle of the explanted hearts of transplant recipients (ischemic and dilated cardiomyopathy), and from nonused donor hearts. Fibroblasts were maintained in culture without passaging for 4 or 8 days (treatment studies). Phenotyping included functional testing, immunostaining, and expression studies for markers of differentiation. These data were complemented with immunohistology and expression studies in tissue samples. Results: Interstitial fibrosis with cross-linked collagen is prominent in HF hearts, with presence of activated MyoFbs. Tissue levels of transforming growth factor (TGF)-β1, lysyl oxidase, periostin, and osteopontin are elevated. Fibroblastic cells isolated from HF hearts are predominantly MyoFb, proliferative or nonproliferative, with mature α-smooth muscle actin stress fibers. HF MyoFb express high levels of profibrotic cytokines and the TGF-β1 pathway is activated. Inhibition of TGF-β1 receptor kinase in HF MyoFb promotes dedifferentiation of MyoFb with loss of α-smooth muscle actin and depolymerization of stress fibers, and reduces the expression of profibrotic genes and cytokines levels to non-HF levels. Conclusion: MyoFb in end-stage HF have a variable degree of differentiation and retain the capacity to return to a less activated state, validating the potential for developing antifibrotic therapy targeting MyoFb.
MeSH term(s)	Cell Adhesion Molecules/analysis ; Cell Differentiation ; Cells, Cultured ; Disease Progression ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosis ; Heart Failure/metabolism ; Heart Failure/pathology ; Humans ; Immunohistochemistry ; Myocardium/metabolism ; Myocardium/pathology ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Osteopontin/analysis ; Protein-Lysine 6-Oxidase/analysis ; Signal Transduction ; Transforming Growth Factor beta1/analysis ; Ventricular Dysfunction/etiology ; Ventricular Dysfunction/metabolism ; Ventricular Dysfunction/pathology
Chemical Substances	Cell Adhesion Molecules ; POSTN protein, human ; Transforming Growth Factor beta1 ; Osteopontin (106441-73-0) ; Protein-Lysine 6-Oxidase (EC 1.4.3.13)
Language	English
Publishing date	2019-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2019.02.049
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Zs.A 1846: 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)
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Article ; Online: Hyperactive ryanodine receptors in human heart failure and ischaemic cardiomyopathy reside outside of couplons.

Dries, Eef / Santiago, Demetrio J / Gilbert, Guillaume / Lenaerts, Ilse / Vandenberk, Bert / Nagaraju, Chandan K / Johnson, Daniel M / Holemans, Patricia / Roderick, H Llewelyn / Macquaide, Niall / Claus, Piet / Sipido, Karin R

Cardiovascular research

2018 Volume 114, Issue 11, Page(s) 1512–1524

Abstract: Aims: In ventricular myocytes from humans and large mammals, the transverse and axial tubular system (TATS) network is less extensive than in rodents with consequently a greater proportion of ryanodine receptors (RyRs) not coupled to this membrane ... ...

Abstract	Aims: In ventricular myocytes from humans and large mammals, the transverse and axial tubular system (TATS) network is less extensive than in rodents with consequently a greater proportion of ryanodine receptors (RyRs) not coupled to this membrane system. TATS remodelling in heart failure (HF) and after myocardial infarction (MI) increases the fraction of non-coupled RyRs. Here we investigate whether this remodelling alters the activity of coupled and non-coupled RyR sub-populations through changes in local signalling. We study myocytes from patients with end-stage HF, compared with non-failing (non-HF), and myocytes from pigs with MI and reduced left ventricular (LV) function, compared with sham intervention (SHAM). Methods and results: Single LV myocytes for functional studies were isolated according to standard protocols. Immunofluorescent staining visualized organization of TATS and RyRs. Ca2+ was measured by confocal imaging (fluo-4 as indicator) and using whole-cell patch-clamp (37°C). Spontaneous Ca2+ release events, Ca2+ sparks, as a readout for RyR activity were recorded during a 15 s period following conditioning stimulation at 2 Hz. Sparks were assigned to cell regions categorized as coupled or non-coupled sites according to a previously developed method. Human HF myocytes had more non-coupled sites and these had more spontaneous activity than in non-HF. Hyperactivity of these non-coupled RyRs was reduced by Ca2+/calmodulin-dependent kinase II (CaMKII) inhibition. Myocytes from MI pigs had similar changes compared with SHAM controls as seen in human HF myocytes. As well as by CaMKII inhibition, in MI, the increased activity of non-coupled sites was inhibited by mitochondrial reactive oxygen species (mito-ROS) scavenging. Under adrenergic stimulation, Ca2+ waves were more frequent and originated at non-coupled sites, generating larger Na+/Ca2+ exchange currents in MI than in SHAM. Inhibition of CaMKII or mito-ROS scavenging reduced spontaneous Ca2+ waves, and improved excitation-contraction coupling. Conclusions: In HF and after MI, RyR microdomain re-organization enhances spontaneous Ca2+ release at non-coupled sites in a manner dependent on CaMKII activation and mito-ROS production. This specific modulation generates a substrate for arrhythmia that appears to be responsive to selective pharmacologic modulation.
MeSH term(s)	Aged ; Animals ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cardiomyopathies/metabolism ; Cardiomyopathies/physiopathology ; Case-Control Studies ; Disease Models, Animal ; Excitation Contraction Coupling ; Female ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Humans ; Male ; Membrane Potentials ; Middle Aged ; Mitochondria, Heart/metabolism ; Myocardial Contraction ; Myocardial Infarction/metabolism ; Myocardial Infarction/physiopathology ; Myocytes, Cardiac/metabolism ; NADPH Oxidase 2/metabolism ; Reactive Oxygen Species/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sodium-Calcium Exchanger/metabolism ; Sus scrofa ; Time Factors ; Ventricular Function, Left ; Ventricular Remodeling
Chemical Substances	Reactive Oxygen Species ; Ryanodine Receptor Calcium Release Channel ; Sodium-Calcium Exchanger ; NADPH Oxidase 2 (EC 1.6.3.-) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)
Language	English
Publishing date	2018-04-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvy088
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Article ; Online: Global fibroblast activation throughout the left ventricle but localized fibrosis after myocardial infarction.

Nagaraju, Chandan K / Dries, Eef / Popovic, Natasa / Singh, Abhishek A / Haemers, Peter / Roderick, H Llewelyn / Claus, Piet / Sipido, Karin R / Driesen, Ronald B

Scientific reports

2017 Volume 7, Issue 1, Page(s) 10801

Abstract: Fibroblast (Fb) differentiation and interstitial fibrosis contribute to cardiac remodeling and loss of function after myocardial infarction (MI). We investigated regional presence and regulation of fibrosis in a pig MI model. In vivo analysis of regional ...

Abstract	Fibroblast (Fb) differentiation and interstitial fibrosis contribute to cardiac remodeling and loss of function after myocardial infarction (MI). We investigated regional presence and regulation of fibrosis in a pig MI model. In vivo analysis of regional function and perfusion defined three regions: the scar, the myocardium adjacent to the scar (MI
MeSH term(s)	Animals ; Cell Differentiation ; Collagen Type I/metabolism ; Disease Models, Animal ; Fibroblasts/physiology ; Fibrosis/pathology ; Gelatinases/metabolism ; Heart Ventricles/pathology ; Membrane Proteins/metabolism ; Myocardial Infarction/complications ; Myocardial Infarction/pathology ; Protein-Lysine 6-Oxidase/metabolism ; Proteoglycans/metabolism ; Serine Endopeptidases/metabolism ; Signal Transduction ; Stress, Mechanical ; Swine ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Collagen Type I ; Membrane Proteins ; Proteoglycans ; Transforming Growth Factor beta1 ; Protein-Lysine 6-Oxidase (EC 1.4.3.13) ; Serine Endopeptidases (EC 3.4.21.-) ; fibroblast activation protein alpha (EC 3.4.21.-) ; Gelatinases (EC 3.4.24.-)
Language	English
Publishing date	2017-09-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-09790-1
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Article ; Online: Reversible and irreversible differentiation of cardiac fibroblasts.

Driesen, Ronald B / Nagaraju, Chandan K / Abi-Char, Joëlle / Coenen, Tamara / Lijnen, Paul J / Fagard, Robert H / Sipido, Karin R / Petrov, Victor V

Cardiovascular research

2013 Volume 101, Issue 3, Page(s) 411–422

Abstract: Aims: Differentiation of cardiac fibroblasts (Fbs) into myofibroblasts (MyoFbs) is responsible for connective tissue build-up in myocardial remodelling. We examined MyoFb differentiation and reversibility.: Methods and results: Adult rat cardiac Fbs ... ...

Abstract	Aims: Differentiation of cardiac fibroblasts (Fbs) into myofibroblasts (MyoFbs) is responsible for connective tissue build-up in myocardial remodelling. We examined MyoFb differentiation and reversibility. Methods and results: Adult rat cardiac Fbs were cultured on a plastic substratum providing mechanical stress, with conditions to obtain different levels of Fb differentiation. Fb spontaneously differentiated to proliferating MyoFb (p-MyoFb) with stress fibre formation decorated with alpha-smooth muscle actin (α-SMA). Transforming growth factor-β1 (TGF-β1) promoted differentiation into α-SMA-positive MyoFb showing near the absence of proliferation, i.e. non-p-MyoFb. SD-208, a TGF-β-receptor-I (TGF-β-RI) kinase blocker, inhibited p-MyoFb differentiation as shown by stress fibre absence, low α-SMA expression, and high proliferation levels. Fb seeded in collagen matrices induced no contraction, whereas p-MyoFb and non-p-MyoFb induced 2.5- and four-fold contraction. Fb produced little collagen but high levels of interleukin-10. Non-p-MyoFb had high collagen production and high monocyte chemoattractant protein-1 and tissue inhibitor of metalloproteinases-1 levels. Transcriptome analysis indicated differential activation of gene networks related to differentiation of MyoFb (e.g. paxilin and PAK) and reduced proliferation of non-p-MyoFb (e.g. cyclins and cell cycle regulation). Dedifferentiation of p-MyoFb with stress fibre de-polymerization, but not of non-p-MyoFb, was induced by SD-208 despite maintained stress. Stress fibre de-polymerization could also be induced by mechanical strain release in p-MyoFb and non-p-MyoFb (2-day cultures in unrestrained 3-D collagen matrices). Only p-MyoFb showed true dedifferentiation after long-term 3-D cultures. Conclusions: Fb, p-MyoFb, and non-p-MyoFb have a distinct gene expression, ultrastructural, and functional profile. Both reduction in mechanical strain and TGF-β-RI kinase inhibition can reverse p-MyoFb differentiation but not non-p-MyoFb.
MeSH term(s)	Animals ; Cell Differentiation/drug effects ; Cell Differentiation/radiation effects ; Cells, Cultured ; Collagen/metabolism ; Gene Expression/drug effects ; Male ; Myofibroblasts/cytology ; Myofibroblasts/metabolism ; Pteridines/pharmacology ; Rats ; Rats, Wistar ; Receptors, Transforming Growth Factor beta/metabolism ; Stress, Physiological ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Pteridines ; Receptors, Transforming Growth Factor beta ; SD-208 ; Transforming Growth Factor beta1 ; Collagen (9007-34-5)
Language	English
Publishing date	2013-12-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvt338
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Article ; Online: Reduced mitochondrial respiration in the ischemic as well as in the remote nonischemic region in postmyocardial infarction remodeling.

Galan, Diogo T / Bito, Virginie / Claus, Piet / Holemans, Patricia / Abi-Char, Joëlle / Nagaraju, Chandan K / Dries, Eef / Vermeulen, Kristel / Ventura-Clapier, Renée / Sipido, Karin R / Driesen, Ronald B

American journal of physiology. Heart and circulatory physiology

2016 Volume 311, Issue 5, Page(s) H1075–H1090

Abstract: Scarring and remodeling of the left ventricle (LV) after myocardial infarction (MI) results in ischemic cardiomyopathy with reduced contractile function. Regional differences related to persisting ischemia may exist. We investigated the hypothesis that ... ...

Abstract	Scarring and remodeling of the left ventricle (LV) after myocardial infarction (MI) results in ischemic cardiomyopathy with reduced contractile function. Regional differences related to persisting ischemia may exist. We investigated the hypothesis that mitochondrial function and structure is altered in the myocardium adjacent to MI with reduced perfusion (MI
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; Animals ; Blotting, Western ; Cardiomyopathies/diagnostic imaging ; Cardiomyopathies/etiology ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cell Respiration ; Cicatrix ; Coronary Stenosis/complications ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Electron Transport Complex IV/metabolism ; Glucose Transport Proteins, Facilitative/genetics ; Glycogen/metabolism ; Magnetic Resonance Imaging ; Microscopy, Electron ; Microscopy, Fluorescence ; Mitochondria, Heart/metabolism ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/etiology ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Perfusion Imaging ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/ultrastructure ; Oxygen Consumption ; RNA, Messenger/metabolism ; Real-Time Polymerase Chain Reaction ; Stroke Volume ; Sus scrofa ; Swine ; Ventricular Remodeling
Chemical Substances	Glucose Transport Proteins, Facilitative ; RNA, Messenger ; Glycogen (9005-79-2) ; Electron Transport Complex II (EC 1.3.5.1) ; Electron Transport Complex IV (EC 1.9.3.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Electron Transport Complex I (EC 7.1.1.2)
Language	English
Publishing date	2016-09-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00945.2015
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Article ; Online: Glycogen synthase kinase-3α/β inhibition promotes in vivo amplification of endogenous mesenchymal progenitors with osteogenic and adipogenic potential and their differentiation to the osteogenic lineage.

Gambardella, Alessandra / Nagaraju, Chandan K / O'Shea, Patrick J / Mohanty, Sindhu T / Kottam, Lucksy / Pilling, James / Sullivan, Michael / Djerbi, Mounira / Koopmann, Witte / Croucher, Peter I / Bellantuono, Ilaria

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2011 Volume 26, Issue 4, Page(s) 811–821

Abstract: Small molecules are attractive therapeutics to amplify and direct differentiation of stem cells. They also can be used to understand the regulation of their fate by interfering with specific signaling pathways. Mesenchymal stem cells (MSCs) have the ... ...

Abstract	Small molecules are attractive therapeutics to amplify and direct differentiation of stem cells. They also can be used to understand the regulation of their fate by interfering with specific signaling pathways. Mesenchymal stem cells (MSCs) have the potential to proliferate and differentiate into several cell types, including osteoblasts. Activation of canonical Wnt signaling by inhibition of glycogen synthase kinase 3 (GSK-3) has been shown to enhance bone mass, possibly by involving a number of mechanisms ranging from amplification of the mesenchymal stem cell pool to the commitment and differentiation of osteoblasts. Here we have used a highly specific novel inhibitor of GSK-3, AR28, capable of inducing β-catenin nuclear translocation and enhanced bone mass after 14 days of treatment in BALB/c mice. We have shown a temporally regulated increase in the number of colony-forming units-osteoblast (CFU-O) and -adipocyte (CFU-A) but not colony-forming units-fibroblast (CFU-F) in mice treated for 3 days. However, the number of CFU-O and CFU-A returned to normal levels after 14 days of treatment, and the number of CFU-F was decreased significantly. In contrast, the number of osteoblasts increased significantly only after 14 days of treatment, and this was seen together with a significant decrease in bone marrow adiposity. These data suggest that the increased bone mass is the result of an early temporal wave of amplification of a subpopulation of MSCs with both osteogenic and adipogenic potential, which is driven to osteoblast differentiation at the expense of adipogenesis.
MeSH term(s)	Acid Phosphatase/metabolism ; Adipocytes/cytology ; Adipocytes/metabolism ; Alkaline Phosphatase/metabolism ; Animals ; Bone Marrow/drug effects ; Bone Marrow Cells/cytology ; Bone Marrow Cells/drug effects ; Calcification, Physiologic/drug effects ; Cell Count ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Line ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell Proliferation/drug effects ; Colony-Forming Units Assay ; Fibroblasts/cytology ; Gene Expression/drug effects ; Gene Expression/genetics ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3 beta ; Isoenzymes/metabolism ; Lipoprotein Lipase/genetics ; Mesenchymal Stromal Cells/cytology ; Mesenchymal Stromal Cells/drug effects ; Mesenchymal Stromal Cells/metabolism ; Mice ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteocalcin/genetics ; Osteoclasts/cytology ; Osteoclasts/metabolism ; Osteogenesis/drug effects ; PPAR gamma/genetics ; Protein Kinase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/pharmacology ; Radiography ; Tartrate-Resistant Acid Phosphatase ; Tibia/anatomy & histology ; Tibia/cytology ; Tibia/diagnostic imaging ; Tibia/drug effects ; beta Catenin/metabolism
Chemical Substances	Isoenzymes ; PPAR gamma ; Protein Kinase Inhibitors ; beta Catenin ; Osteocalcin (104982-03-8) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; glycogen synthase kinase 3 alpha (EC 2.7.11.26) ; Lipoprotein Lipase (EC 3.1.1.34) ; Alkaline Phosphatase (EC 3.1.3.1) ; Acid Phosphatase (EC 3.1.3.2) ; Tartrate-Resistant Acid Phosphatase (EC 3.1.3.2)
Language	English
Publishing date	2011-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.266
Database	MEDical Literature Analysis and Retrieval System OnLINE

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