Neuronal Nitric Oxide Synthase Protects Against Myocardial Infarction-Induced Ventricular Arrhythmia and Mortality in Mice

Burger, Dylan; Lu, Xiangru; Lei, Ming; Xiang, Fu-Li; Hammoud, Lamis; Jiang, Mao; Wang, Hao; Jones, Douglas L.; Sims, Stephen M.; Feng, Qingping

doi:10.1161/circulationaha.108.846402

Cited by 114 publications

(114 citation statements)

References 33 publications

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“…The SDS concentration in the lysate was then adjusted to 0.2% SDS before 30-min incubation at room temperature with intermittent vortexing. After centrifugation (2500 relative centrifugal force for 5 min), the fluorescence in the lysate was measured using a Spectramax M5 multimode plate reader (Molecular Devices; excitation, 500 nm; emission, 535 nm; cutoff at 515 nm; number of reads, 20). From this point on, the samples were protected from light.…”

Section: Methodsmentioning

confidence: 99%

“…A previous study indicates that the Cys-289 site in the CaMKII␣ isoform has a role in oxidation-induced activation of the kinase (16). Because the balance of oxidation and nitrosylation is thought to play a key role in cardiovascular signaling (20), we sought to determine whether the Cys-290 site was similarly subject to oxidative effects in CaMKII␦. Therefore, we also measured the effects of 1 M H 2 O 2 on the CaMKII␦ mutant forms of Camui.…”

Section: No-induced Camkii␦ Activation Is Dependent On the Cys-290mentioning

confidence: 99%

“…Moreover, CaMKII␦ is already known to be activated by oxidative stress (9), and perturbations of the balance between the nitroso and redox levels in the heart are thought to play a key role in cardiovascular pathology (20). Therefore, establishing the mechanism by which NO activates CaMKII␦ is critical for elucidating the underlying connection between NO signaling and cardiac function.…”

mentioning

confidence: 99%

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S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

Erickson

Nichols

Uchinoumi

et al. 2015

Journal of Biological Chemistry

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Background: CaMKII␦ and NO can modulate cardiac signaling/pathology. Results: NO treatment after calcium/calmodulin binding prolongs CaMKII␦ activation, whereas NO pretreatment inhibits CaMKII␦ activation, effects mediated by Cys-290 and Cys-273, respectively. Conclusion: S-nitrosylation has a dual role in modulating CaMKII␦ in the heart. Significance: Dual regulation by NO is a new pathway by which CaMKII can modulate cardiac function.

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Section: Methodsmentioning

confidence: 99%

Section: No-induced Camkii␦ Activation Is Dependent On the Cys-290mentioning

confidence: 99%

mentioning

confidence: 99%

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S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

Erickson

Nichols

Uchinoumi

et al. 2015

Journal of Biological Chemistry

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“…In addition, the catalytic activity and subcellular localization of eNOS are governed by a complex series of interactions with other proteins [17][18][19][20][21][22][23][24], phosphorylation [25,26], and palmitoylation [24,[27][28][29].…”

Section: Introductionmentioning

confidence: 99%

Triacsin C, a Fatty Acyl CoA Synthetase Inhibitor, Improves Cardiac Performance Following Global Ischemia

Blakeman¹,

Chen²,

Tolson³

et al. 2012

Am. J. Biomed. Sci.

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The role of fatty acyl CoA synthetase (FACS) in ischemia/reperfusion (I/R) injury has not been well established. Our earlier studies showed that triacsin C, a selective FACS inhibitor, decreases endothelial nitric oxide synthase (eNOS) palmitoylation and increases nitric oxide (NO) in cultured human coronary endothelial cells. In the present study, we tested the hypothesis that triacsin C would reduce infarct size and improve post-reperfusion cardiac function by increasing vascular NO. In isolated rat hearts, triacsin C, given during the first 5 minutes of reperfusion, significantly reduced infarct size and attenuated cardiac dysfunction during reperfusion. N G -nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 50 µM) completely abolished the protective effects of triacsin C. In the ischemic hind limb model, triacsin C significantly increased intravascular NO concentration during reperfusion, an effect that was blocked by L-NAME or S-methyl-L-thiocitrulline (SMTC, a selective neuronal NOS inhibitor), but not by 1400W (a highly selective iNOS inhibitor). Lastly, triacsin C significantly reduced L-NAME induced leukocyte rolling, adhesion, and transmigration in rat mesenteric circulation, as measured by intravital microscopy. In summary, this study provides novel evidence showing that triacsin C reduces myocardial infarct size, attenuates loss of post-reperfusion cardiac function, increases intravascular NO concentration and inhibits leukocyte recruitment. These pharmacologic properties suggest that triacsin C may be useful as an adjunct to Am.

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“…The function of nNO remains under investigation but in the heart it regulates chronotropicity and may play a protective role in the myocardial response to injury. (16)(17)(18)(19)(20)(21) …”

Section: Introductionmentioning

confidence: 99%

Targeting the Endothelium

Adams

2010

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Neuronal Nitric Oxide Synthase Protects Against Myocardial Infarction-Induced Ventricular Arrhythmia and Mortality in Mice

Cited by 114 publications

References 33 publications

S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

Triacsin C, a Fatty Acyl CoA Synthetase Inhibitor, Improves Cardiac Performance Following Global Ischemia

Targeting the Endothelium

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