Cardiac-specific overexpression of catalase rescues ventricular myocytes from ethanol-induced cardiac contractile defect

Zhang, Xiaochun; Klein, Aaron L.; Alberle, Nicholas S.; Norby, Faye L.; Ren, Bonnie H.; Duan, Jiaqi; Ren, Jun

doi:10.1016/s0022-2828(03)00080-4

Cited by 65 publications

(66 citation statements)

References 37 publications

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“…Four-month-old male FVB and catalase-transgenic mice (∼18 g) were fed either a cornstarch or sucrose (each providing 68% of total energy) diet (Research Diets, New Brunswick, NJ, USA) for 12 weeks. Generation and identification of cardiac-specific catalase-transgenic mice were described previously [20,21]. A primer pair derived from the myosin heavy chain promoter and rat catalase cDNA was used with the reverse sequence of aat atc gtg ggt gac ctc aa and the forward sequence of cag atg aag cag tgg aag ga. A line with cardiac catalase activity of 1,456 μmol min −1 mg −1 protein or 60-fold of that of the wild-type mouse was used in this study.…”

Section: Experimental Animals and Induction Of Whole-body Insulin Resmentioning

confidence: 99%

“…Fresh myocytes were used within 8 h. Cell viability was approximately 70% in all animal groups. Only rod-shaped myocytes with clear edges were selected for recording of mechanical properties [21].…”

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

“…Cell shortening/relengthening measurements Mechanical properties of cardiomyocytes were assessed using a SoftEdge MyoCam system (IonOptix Corporation, Milton, MA, USA) [21]. Cell shortening and relengthening were assessed using the following indices: peak shortening (PS), time-to-PS (TPS) and time-to-90% relengthening (TR 90 ), half-width duration (HWD), which reflects the duration from 50% shortening to 50% relengthening, and maximal velocities of shortening (+dL/dt) and relengthening (−dL/dt).…”

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

“…Qualitative changes in intracellular Ca 2+ concentration were inferred from the ratio of the fura-2 fluorescence intensity (FFI) at two wavelengths. Fluorescence decay time was also measured as an indication of the intracellular Ca 2+ clearing rate [21].…”

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

“…After removal of excess primary antibody binding, blots were incubated for 1 h with horseradish peroxidase-conjugated secondary antibody. Antibody binding was detected using enhanced chemiluminescence and films were evaluated with a Bio-Rad Calibrated Densitometer [21].…”

Section: Protein Carbonyl Assaymentioning

confidence: 99%

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Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

et al. 2006

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Aims/hypothesis: Insulin resistance leads to oxidative stress and cardiac dysfunction. This study examined the impact of catalase on insulin-resistanceinduced cardiac dysfunction, oxidative damage and insulin sensitivity. Methods: Insulin resistance was initiated in FVB and catalase-transgenic mice by 12 weeks of sucrose feeding. Contractile and intracellular Ca 2+ properties were evaluated in cardiomyocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR 90 ), half-width duration (HWD), maximal velocity of shortening/relengthening (±dL/dt), fura-fluorescence intensity change (ΔFFI) and intracellular Ca 2+ clearance rate (τ). Reactive oxygen species (ROS) and protein damage were evaluated with dichlorodihydrofluorescein and protein carbonyl formation. Results: Sucrose-fed mice displayed hyperinsulinaemia, impaired glucose tolerance and normal body weight. Myocytes from FVB sucrose-fed mice exhibited depressed PS and ±dL/dt, prolonged TR 90 and τ, and reduced ΔFFI associated with normal TPS and HWD compared with those from starch-fed control mice. ROS and protein carbonyl formation were elevated in FVB sucrose-fed mice. Insulin sensitivity was reduced, evidenced by impaired insulin-stimulated 2-deoxy-D-[ 3 H] glucose uptake. Western blot analysis indicated that sucrose feeding: (1) inhibited insulin-stimulated phosphorylation of insulin receptor and Akt; (2) enhanced proteintyrosine phosphatase 1B (PTP1B) expression; and (3) suppressed endothelial nitric oxide synthase (eNOS) and Na + -Ca 2+ exchanger expression without affecting peroxisome proliferator-activated receptor γ (PPARγ), sarco(endo)plasmic reticulum Ca 2+ -ATPase isozyme 2a and phospholamban. Catalase ablated insulin-resistanceinduced mechanical dysfunction, ROS production and protein damage, and reduced eNOS, but not insulin insensitivity. Catalase itself decreased resting FFI and enhanced expression of PTP1B and PPARγ. Conclusions/ interpretation: These data indicate that catalase rescues insulin-resistance-induced cardiac dysfunction related to ROS production and protein oxidation but probably does not improve insulin sensitivity.

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Section: Experimental Animals and Induction Of Whole-body Insulin Resmentioning

confidence: 99%

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

Section: Isolation Of Mouse Ventricular Myocytesmentioning

confidence: 99%

Section: Protein Carbonyl Assaymentioning

confidence: 99%

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Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

et al. 2006

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Reactive oxygen species and peroxisomes: Struggling for balance

et al. 2009

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Reactive oxygen species (ROS) can surely be considered as multifunctional biofactors within the cell. They are known to participate in regular cell functions, for example, as signal mediators, but overproduction under oxidative stress conditions leads to deleterious cellular effects, cell death and diverse pathological conditions. Peroxisomal function has long been linked to oxygen metabolism due to the high concentration of H(2)O(2)-generating oxidases in peroxisomes and their set of antioxidant enzymes, especially catalase. Still, mitochondria have been very much placed in the centre of ROS metabolism and oxidative stress. This review discusses novel findings concerning the relationship between ROS and peroxisomes, as they revealed to be a key player in the dynamic spin of ROS metabolism and oxidative injury. An overview of ROS generating enzymes as well as their antioxidant counterparts will be given, exemplifying the precise fine-tuning between the opposing systems. Various conditions in which the balance between generation and scavenging of ROS in peroxisomes is perturbed, for example, exogenous manipulation, ageing and peroxisomal disorders, are addressed. Furthermore, peroxisome-derived oxidative stress and its effect on mitochondria (and vice versa) are discussed, highlighting the close interrelationship of both organelles.

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PDE5 inhibitor sildenafil attenuates cardiac microRNA 214 upregulation and pro-apoptotic signaling after chronic alcohol ingestion in mice

Samidurai

Salloum

et al. 2020

Mol Cell Biochem

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Cardiac-specific overexpression of catalase rescues ventricular myocytes from ethanol-induced cardiac contractile defect

Cited by 65 publications

References 37 publications

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

Reactive oxygen species and peroxisomes: Struggling for balance

PDE5 inhibitor sildenafil attenuates cardiac microRNA 214 upregulation and pro-apoptotic signaling after chronic alcohol ingestion in mice

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