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Article ; Online: Time and charge/pH-dependent activation of K+ channel-mediated K+ influx and K+/H+ exchange in guinea pig heart isolated mitochondria; role in bioenergetic stability.

Malas, Kareem M / Lambert, David S / Heisner, James S / Camara, Amadou K S / Stowe, David F

Biochimica et biophysica acta. Bioenergetics

2022 Volume 1863, Issue 8, Page(s) 148908

Abstract: Mitochondria play an important role not only in producing energy for the cell but also for regulating mitochondrial and cell function depending on the cell's needs and environment. Uptake of cations, anions, and substrates requires a stable, polarized ... ...

Abstract	Mitochondria play an important role not only in producing energy for the cell but also for regulating mitochondrial and cell function depending on the cell's needs and environment. Uptake of cations, anions, and substrates requires a stable, polarized transmembrane charge potential (ΔΨ<sub>m</sub>). Chemiosmosis requires ion exchangers to remove Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup>, PO<sub>4</sub><sup>3-</sup>, and other charged species that enter mitochondria. Knowledge of the kinetics of mitochondrial (m) cation channels and exchangers is important in understanding their roles in regulating mitochondrial chemiosmosis and bioenergetics. The influx/efflux of K<sup>+</sup>, the most abundant mitochondrial cation, alters mitochondrial volume and shape by bringing in anions and H<sub>2</sub>O by osmosis. The effects of K<sup>+</sup> uptake through ligand-specific mK<sup>+</sup> channels stimulated/inhibited by agonists/antagonists on mitochondrial volume (swelling/contraction) are well known. However, a more important role for K<sup>+</sup> influx is likely its effects on H<sup>+</sup> cycling and bioenergetics facilitated by mitochondrial (m) K<sup>+</sup>/H<sup>+</sup> exchange (mKHE), though the kinetics and consequences of K<sup>+</sup> efflux by KHE are not well described. We hypothesized that a major role of K<sup>+</sup> influx/efflux is stimulation of respiration via the influx of H<sup>+</sup> by KHE. We proposed to modulate KHE activity by energizing guinea pig heart isolated mitochondria and by altering the mK<sup>+</sup> cycle to capture changes in mitochondrial volume, pH<sub>m</sub>, ΔΨ<sub>m</sub>, and respiration that would reflect a role for H<sup>+</sup> influx via KHE to regulate bioenergetics. To test this, mitochondria were suspended in a 150 mM K<sup>+</sup> buffer at pH 6.9, or in a 140 mM Cs<sup>+</sup> buffer at pH 7.6 or 6.9 with added 10 mM K<sup>+</sup>, minimal Ca<sup>2+</sup> and free of Na<sup>+</sup>. O<sub>2</sub> content was measured by a Clark electrode, and pH<sub>m</sub>, ΔΨ<sub>m</sub>, and volume, were measured by fluorescence spectrophotometry and light-scattering. Adding pyruvic acid (PA) alone caused increases in volume and respiration and a rapid decrease in the transmembrane pH gradient (ΔpH<sub>m</sub> = pH<sub>in</sub>-pH<sub>ext</sub>) at pH<sub>ext</sub> 6.9> > 7.6, so that ΔΨ<sub>m</sub> was charged and maintained. BK<sub>Ca</sub> agonist NS1619 and antagonist paxilline modified these effects, and KHE inhibitor quinine and K<sup>+</sup> ionophore valinomycin depolarized ΔΨ<sub>m</sub>. We postulate that K<sup>+</sup> efflux-induced H<sup>+</sup> influx via KHE causes an inward H<sup>+</sup> leak that stimulates respiration, but at buffer pH 6.9 also utilizes the energy of ΔpH<sub>m</sub>, the smaller component of the overall proton motive force, ΔμH<sup>+</sup>. Thus ΔpH<sub>m</sub> establishes and maintains the ΔΨ<sub>m</sub> required for utilization of substrates, entry of all cations, and for oxidative phosphorylation. Thus, K<sup>+</sup> influx/efflux appears to play a pivotal role in regulating energetics while maintaining mitochondrial ionic balance and volume homeostasis.
MeSH term(s)	Animals ; Anions/metabolism ; Energy Metabolism ; Guinea Pigs ; Hydrogen-Ion Concentration ; Ionophores/metabolism ; Ionophores/pharmacology ; Ligands ; Mitochondria, Heart/metabolism ; Potassium/metabolism ; Pyruvic Acid/metabolism ; Pyruvic Acid/pharmacology ; Quinine/metabolism ; Quinine/pharmacology ; Valinomycin/metabolism ; Valinomycin/pharmacology
Chemical Substances	Anions ; Ionophores ; Ligands ; Valinomycin (2001-95-8) ; Pyruvic Acid (8558G7RUTR) ; Quinine (A7V27PHC7A) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2022-08-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	60-7
ISSN	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbabio.2022.148908
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Article ; Online: Single-lung ventilation and oxidative stress: a different perspective on a common practice.

Heerdt, Paul M / Stowe, David F

Current opinion in anaesthesiology

2017 Volume 30, Issue 1, Page(s) 42–49

Abstract: Purpose of review: To summarize what is currently known about the relationship between single-lung ventilation (SLV), oxidative stress, and postoperative disruption of organ function.: Recent findings: SLV produces progressive alelectasis that is ... ...

Abstract	Purpose of review: To summarize what is currently known about the relationship between single-lung ventilation (SLV), oxidative stress, and postoperative disruption of organ function. Recent findings: SLV produces progressive alelectasis that is associated with hypoxic pulmonary vasoconstriction and redistribution of blood flow away from the nonventilated lung. This local tissue hypoxia induces the generation of reactive oxygen and reactive nitrogen species, an effect subsequently amplified by lung re-expansion consistent with well described hypoxia/reperfusion responses. Both experimental and clinical data indicate that the magnitude of oxidative and nitrosative stress is related to the duration of SLV and that these stresses affect not only the collapsed/re-expanded lung, but other organs as well. Summary: SLV and subsequent re-expansion of atelectatic lung are associated with the generation of reactive oxygen and nitrogen species that may modulate persistent systemic effects.
MeSH term(s)	Animals ; Antioxidants/therapeutic use ; Humans ; Lung/blood supply ; Lung/metabolism ; Lung/physiopathology ; Models, Animal ; One-Lung Ventilation/adverse effects ; One-Lung Ventilation/methods ; Oxidative Stress ; Postoperative Complications/etiology ; Postoperative Complications/prevention & control ; Pulmonary Atelectasis/etiology ; Pulmonary Atelectasis/physiopathology ; Reactive Oxygen Species/metabolism ; Regional Blood Flow ; Reperfusion Injury/etiology ; Reperfusion Injury/physiopathology ; Reperfusion Injury/prevention & control ; Thoracic Surgical Procedures/adverse effects ; Time Factors
Chemical Substances	Antioxidants ; Reactive Oxygen Species
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645203-6
ISSN	1473-6500 ; 0952-7907
ISSN (online)	1473-6500
ISSN	0952-7907
DOI	10.1097/ACO.0000000000000410
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Article ; Online: Hypothermia Prevents Cardiac Dysfunction during Acute Ischemia Reperfusion by Maintaining Mitochondrial Bioenergetics and by Promoting Hexokinase II Binding to Mitochondria.

Sun, Jie / Mishra, Jyotsna / Yang, Meiying / Stowe, David F / Heisner, James S / An, Jianzhong / Kwok, Wai-Meng / Camara, Amadou K S

Oxidative medicine and cellular longevity

2022 Volume 2022, Page(s) 4476448

Abstract: Background: Hypothermia (H), cardioplegia (CP), and both combined (HCP) are known to be protective against myocardial ischemia reperfusion (IR) injury. Mitochondria have molecular signaling mechanisms that are associated with both cell survival and cell ...

Abstract	Background: Hypothermia (H), cardioplegia (CP), and both combined (HCP) are known to be protective against myocardial ischemia reperfusion (IR) injury. Mitochondria have molecular signaling mechanisms that are associated with both cell survival and cell death. In this study, we investigated the dynamic changes in proapoptotic and prosurvival signaling pathways mediating H, CP, or HCP-induced protection of mitochondrial function after acute myocardial IR injury. Methods: Rats were divided into five groups. Each group consists of 3 subgroups based on a specific reperfusion time (5, 20, or 60 min) after a 25-min global ischemia. The time control (TC) groups were not subjected to IR but were perfused with 37 °C Krebs-Ringer's (KR) buffer, containing 4.5 mM K Results: H and HCP were more protective of mitochondrial integrity and, concomitantly, cardiac function than CP alone; H and HCP improved post-ischemic cardiac function by (1) maintaining mitochondrial bioenergetics, (2) maintaining HKII binding to mitochondria with an increase in pAkt levels, (3) increasing CRC, and (4) decreasing Cyto- Conclusions: Hypothermia preserved mitochondrial function and cardiac function, in part, by maintaining mitochondrial bioenergetics, by retaining HKII binding to mitochondria via upstream pAkt, and by reducing Cyto-
MeSH term(s)	Animals ; Energy Metabolism ; Hexokinase/metabolism ; Hypothermia/metabolism ; Ischemia/metabolism ; Mitochondria/metabolism ; Mitochondria, Heart/metabolism ; Myocardial Reperfusion Injury/metabolism ; Rats ; Reperfusion ; bcl-2-Associated X Protein/metabolism
Chemical Substances	bcl-2-Associated X Protein ; Hexokinase (EC 2.7.1.1)
Language	English
Publishing date	2022-07-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2022/4476448
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Article: Time and charge/pH-dependent activation of K+ channel-mediated K+ influx and K+/H+ exchange in guinea pig heart isolated mitochondria; role in bioenergetic stability

Malas, Kareem M. / Lambert, David S. / Heisner, James S. / Camara, Amadou K.S. / Stowe, David F.

Biochimica et biophysica acta. 2022 Nov. 01, v. 1863, no. 8

2022

Abstract	Mitochondria play an important role not only in producing energy for the cell but also for regulating mitochondrial and cell function depending on the cell's needs and environment. Uptake of cations, anions, and substrates requires a stable, polarized transmembrane charge potential (ΔΨₘ). Chemiosmosis requires ion exchangers to remove Na⁺, K⁺, Ca²⁺, PO₄³⁻, and other charged species that enter mitochondria. Knowledge of the kinetics of mitochondrial (m) cation channels and exchangers is important in understanding their roles in regulating mitochondrial chemiosmosis and bioenergetics. The influx/efflux of K⁺, the most abundant mitochondrial cation, alters mitochondrial volume and shape by bringing in anions and H₂O by osmosis. The effects of K⁺ uptake through ligand-specific mK⁺ channels stimulated/inhibited by agonists/antagonists on mitochondrial volume (swelling/contraction) are well known. However, a more important role for K⁺ influx is likely its effects on H⁺ cycling and bioenergetics facilitated by mitochondrial (m) K⁺/H⁺ exchange (mKHE), though the kinetics and consequences of K⁺ efflux by KHE are not well described. We hypothesized that a major role of K⁺ influx/efflux is stimulation of respiration via the influx of H⁺ by KHE. We proposed to modulate KHE activity by energizing guinea pig heart isolated mitochondria and by altering the mK⁺ cycle to capture changes in mitochondrial volume, pHₘ, ΔΨₘ, and respiration that would reflect a role for H⁺ influx via KHE to regulate bioenergetics. To test this, mitochondria were suspended in a 150 mM K⁺ buffer at pH 6.9, or in a 140 mM Cs⁺ buffer at pH 7.6 or 6.9 with added 10 mM K⁺, minimal Ca²⁺ and free of Na⁺. O₂ content was measured by a Clark electrode, and pHₘ, ΔΨₘ, and volume, were measured by fluorescence spectrophotometry and light-scattering. Adding pyruvic acid (PA) alone caused increases in volume and respiration and a rapid decrease in the transmembrane pH gradient (ΔpHₘ = pHᵢₙ–pHₑₓₜ) at pHₑₓₜ 6.9> > 7.6, so that ΔΨₘ was charged and maintained. BKCₐ agonist NS1619 and antagonist paxilline modified these effects, and KHE inhibitor quinine and K⁺ ionophore valinomycin depolarized ΔΨₘ. We postulate that K⁺ efflux-induced H⁺ influx via KHE causes an inward H⁺ leak that stimulates respiration, but at buffer pH 6.9 also utilizes the energy of ΔpHₘ, the smaller component of the overall proton motive force, ΔμH⁺. Thus ΔpHₘ establishes and maintains the ΔΨₘ required for utilization of substrates, entry of all cations, and for oxidative phosphorylation. Thus, K⁺ influx/efflux appears to play a pivotal role in regulating energetics while maintaining mitochondrial ionic balance and volume homeostasis.
Keywords	agonists ; antagonists ; buffer index ; calcium ; cations ; electrodes ; energy ; fluorescence emission spectroscopy ; guinea pigs ; heart ; homeostasis ; light scattering ; mitochondria ; osmosis ; oxidative phosphorylation ; pH ; paxilline ; proton-motive force ; pyruvic acid ; quinine ; valinomycin
Language	English
Dates of publication	2022-1101
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	282711-6
ISSN	0005-2728 ; 0304-4173
ISSN	0005-2728 ; 0304-4173
DOI	10.1016/j.bbabio.2022.148908
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Inflammatory-associated proteomic predictors of cognitive outcome in subjects with ELVO treated by mechanical thrombectomy.

Maglinger, Benton / Harp, Jordan P / Frank, Jacqueline A / Rupareliya, Chintan / McLouth, Christopher J / Pahwa, Shivani / Sheikhi, Lila / Dornbos, David / Trout, Amanda L / Stowe, Ann M / Fraser, Justin F / Pennypacker, Keith R

BMC neurology

2023 Volume 23, Issue 1, Page(s) 214

Abstract: Background: Emergent Large Vessel Occlusion (ELVO) stroke causes devastating vascular events which can lead to significant cognitive decline and dementia. In the subset of ELVO subjects treated with mechanical thrombectomy (MT) at our institution, we ... ...

Abstract	Background: Emergent Large Vessel Occlusion (ELVO) stroke causes devastating vascular events which can lead to significant cognitive decline and dementia. In the subset of ELVO subjects treated with mechanical thrombectomy (MT) at our institution, we aimed to identify systemic and intracranial proteins predictive of cognitive function at time of discharge and at 90-days. These proteomic biomarkers may serve as prognostic indicators of recovery, as well as potential targets for novel/existing therapeutics to be delivered during the subacute stage of stroke recovery. Methods: At the University of Kentucky Center for Advanced Translational Stroke Sciences, the BACTRAC tissue registry (clinicaltrials.gov; NCT03153683) of human biospecimens acquired during ELVO stroke by MT is utilized for research. Clinical data are collected on each enrolled subject who meets inclusion criteria. Blood samples obtained during thrombectomy were sent to Olink Proteomics for proteomic expression values. Montreal Cognitive Assessments (MoCA) were evaluated with categorical variables using ANOVA and t-tests, and continuous variables using Pearson correlations. Results: There were n = 52 subjects with discharge MoCA scores and n = 28 subjects with 90-day MoCA scores. Several systemic and intracranial proteins were identified as having significant correlations to discharge MoCA scores as well as 90-day MoCA scores. Highlighted proteins included s-DPP4, CCL11, IGFBP3, DNER, NRP1, MCP1, and COMP. Conclusion: We set out to identify proteomic predictors and potential therapeutic targets related to cognitive outcomes in ELVO subjects undergoing MT. Here, we identify several proteins which predicted MoCA after MT, which may serve as therapeutic targets to lessen post-stroke cognitive decline.
MeSH term(s)	Humans ; Brain Ischemia ; Proteomics ; Treatment Outcome ; Stroke ; Thrombectomy ; Arterial Occlusive Diseases ; Ischemic Stroke ; Retrospective Studies
Language	English
Publishing date	2023-06-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2041347-6
ISSN	1471-2377 ; 1471-2377
ISSN (online)	1471-2377
ISSN	1471-2377
DOI	10.1186/s12883-023-03253-z
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Article: Editorial: Genetic Modification of Cardiac Tissue.

Camara, Amadou K S / Stowe, David F / O-Uchi, Jin / Bazil, Jason N

Frontiers in cardiovascular medicine

2019 Volume 6, Page(s) 93

Language	English
Publishing date	2019-07-16
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2019.00093
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Article ; Online: Modulation of peroxynitrite produced via mitochondrial nitric oxide synthesis during Ca

Gerdes, Harrison J / Yang, Meiying / Heisner, James S / Camara, Amadou K S / Stowe, David F

Biochimica et biophysica acta. Bioenergetics

2020 Volume 1861, Issue 12, Page(s) 148290

Abstract: We hypothesized that ... ...

Abstract	We hypothesized that NO
MeSH term(s)	Animals ; Calcium/pharmacology ; Electron Transport/drug effects ; Free Radical Scavengers/metabolism ; Guinea Pigs ; Hydrogen Peroxide/metabolism ; Isoenzymes/metabolism ; Isoenzymes/ultrastructure ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/ultrastructure ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase/ultrastructure ; Oxidative Stress/drug effects ; Peroxynitrous Acid/metabolism ; Spectrometry, Fluorescence ; Stress, Physiological/drug effects ; Succinic Acid/pharmacology ; Superoxide Dismutase/metabolism ; Time Factors
Chemical Substances	Free Radical Scavengers ; Isoenzymes ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; Succinic Acid (AB6MNQ6J6L) ; Hydrogen Peroxide (BBX060AN9V) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Superoxide Dismutase (EC 1.15.1.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-08-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	60-7
ISSN	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbabio.2020.148290
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Article ; Online: Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.

Yang, Meiying / Sun, Jie / Stowe, David F / Tajkhorshid, Emad / Kwok, Wai-Meng / Camara, Amadou K S

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2020 Volume 54, Issue 5, Page(s) 853–874

Abstract: Background/aims: The role of VDAC1, the most abundant mitochondrial outer membrane protein, in cell death depends on cell types and stimuli. Both silencing and upregulation of VDAC1 in various type of cancer cell lines can stimulate apoptosis. In ... ...

Abstract	Background/aims: The role of VDAC1, the most abundant mitochondrial outer membrane protein, in cell death depends on cell types and stimuli. Both silencing and upregulation of VDAC1 in various type of cancer cell lines can stimulate apoptosis. In contrast, in mouse embryonic stem (MES) cells and mouse embryonic fibroblasts (MEFs), the roles of VDAC1 knockout (VDAC1 Methods: We knocked out VDAC1 in this rat cardiomyoblast cell line with CRISPR-Cas9 genome editing technique to produce VDAC1 Results: We found that under control conditions, VDAC1 Conclusion: Our results suggest that VDAC1
MeSH term(s)	Animals ; Apoptosis/physiology ; Cell Line ; Cell Proliferation/physiology ; Cell Survival/immunology ; Gene Knockout Techniques ; Glycolysis ; Hexokinase/metabolism ; Mitochondria/enzymology ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism ; Myocytes, Cardiac/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Rats ; Signal Transduction ; Voltage-Dependent Anion Channel 1/genetics ; Voltage-Dependent Anion Channel 1/metabolism ; tert-Butylhydroperoxide/pharmacology
Chemical Substances	Vdac1 protein, rat ; tert-Butylhydroperoxide (955VYL842B) ; Voltage-Dependent Anion Channel 1 (EC 1.6.-) ; Hexokinase (EC 2.7.1.1)
Keywords	covid19
Language	English
Publishing date	2020-09-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.33594/000000274
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Article ; Online: PPARγ-Independent Side Effects of Thiazolidinediones on Mitochondrial Redox State in Rat Isolated Hearts.

Riess, Matthias L / Elorbany, Reem / Weihrauch, Dorothee / Stowe, David F / Camara, Amadou K S

Cells

2020 Volume 9, Issue 1

Abstract: The effect of anti-diabetic thiazolidinediones (TZDs) on contributing to heart failure and cardiac ischemia/reperfusion (IR) injury is controversial. In this study we investigated the effect of select TZDs on myocardial and mitochondrial function in ... ...

Abstract	The effect of anti-diabetic thiazolidinediones (TZDs) on contributing to heart failure and cardiac ischemia/reperfusion (IR) injury is controversial. In this study we investigated the effect of select TZDs on myocardial and mitochondrial function in Brown Norway rat isolated hearts. In a first set of experiments, the TZD rosiglitazone was given acutely before global myocardial IR, and pre- and post-IR function and infarct size were assessed. In a second set of experiments, different concentrations of rosiglitazone and pioglitazone were administered in the presence or absence of the specific PPARγ antagonist GW9662, and their effects on the mitochondrial redox state were measured by online NADH and FAD autofluorescence. The administration of rosiglitazone did not significantly affect myocardial function except for transiently increasing coronary flow, but it increased IR injury compared to the control hearts. Both TZDs resulted in dose-dependent, reversible increases in mitochondrial oxidation which was not attenuated by GW9662. Taken together, these data suggest that TZDs cause excessive mitochondrial uncoupling by a PPARγ-independent mechanism. Acute rosiglitazone administration before IR was associated with enhanced cardiac injury. If translated clinically, susceptible patients on PPARγ agonists may experience enhanced myocardial IR injury by mitochondrial dysfunction.
MeSH term(s)	Animals ; Flavin-Adenine Dinucleotide/metabolism ; Fluorescence ; Male ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/metabolism ; Myocardial Reperfusion Injury/pathology ; NAD/metabolism ; Oxidation-Reduction ; PPAR gamma/metabolism ; Rats, Inbred BN ; Thiazolidinediones/pharmacology
Chemical Substances	PPAR gamma ; Thiazolidinediones ; NAD (0U46U6E8UK) ; Flavin-Adenine Dinucleotide (146-14-5)
Language	English
Publishing date	2020-01-20
Publishing country	Switzerland
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	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9010252
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Article: Total Matrix Ca

Natarajan, Gayathri K / Glait, Lyall / Mishra, Jyotsna / Stowe, David F / Camara, Amadou K S / Kwok, Wai-Meng

Frontiers in physiology

2020 Volume 11, Page(s) 510600

Abstract: Mitochondrial ... ...

Abstract	Mitochondrial Ca
Language	English
Publishing date	2020-09-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2020.510600
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