Protein Kinase C Isoform (PKC) Peptide Activator/Inhibitors Exert Cardioprotective Effects in Polymorphonuclear Leukocyte (PMN)-induced Ischemia/Reperfusion (I/R) Injury

Young, Lindon H.; Phillipson, Aisha; Omiyi, Didi; Atkinson, Norrell; Jivani, M.; Adams, Jovan; Peterman, Ellen E.

doi:10.1007/978-0-387-26575-9_194

Cited by 2 publications

(3 citation statements)

References 2 publications

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“…Doing so facilitates study of the process in the intact animal. Several publications have shown that the isolated rat aortic segment model is a prognostic indicator of whole organ function (15,(24)(25)(26)(27). Overall, the experimental setup is cost effective in that small amount of reagents, tissues, or cells are needed to generate reliable data.…”

Section: Discussionmentioning

confidence: 99%

“…At the conclusion of the experiment, the aortic segments are blotted and weighed, and results are usually reported as moles of NO released per gram of tissue (15,(23)(24)(25)(26)(27). Figure 3A is an illustration depicting the experimental setup for rat aortic segment tissue.…”

Section: Methodsmentioning

confidence: 99%

“…Real-time measurement of H 2 O 2 and NO can also be performed on isolated tissue bathed in physiologic buffers or on cultured cells in tissue culture medium (15,(22)(23)(24)(25)(26)(27). Previous studies have even utilized electrodes in organ chambers to record NO concentration (28).…”

Section: In Vitro Applicationsmentioning

confidence: 99%

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Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Young

Chen²,

Weis³

2011

Am. J. Biomed. Sci.

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Vascular endothelial dysfunction is a common and early event occurring in many disease conditions, such as ischemia/reperfusion (I/R) injury, vascular complications of diabetes, and clinical procedures that injure blood vessels. The hallmark of endothelial dysfunction is reduced bioavailability of nitric oxide (NO) and consequent increased free radical production. These radicals trigger the inflammatory response, a major contributor to tissue injury. Measuring free radical release in biological models facilitates assessment of the biochemical mechanisms responsible for regulating the production of these biomolecules. This technical review focuses on the application of real-time measurement of hydrogen peroxide (H 2 O 2 ) and NO release in models of I/R and blood vessel injury. The technique presents a valuable tool to study not only NO/H 2 O 2 release, but also to identify novel pharmacologic agents modifying that release.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Young

Chen²,

Weis³

2011

Am. J. Biomed. Sci.

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Mechanisms related to the cardioprotective effects of protein kinase C epsilon (PKC ɛ) peptide activator or inhibitor in rat ischemia/reperfusion injury

Teng

Kay

Chen

et al. 2008

Naunyn-Schmied Arch Pharmacol

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The role of protein kinase C epsilon (PKC epsilon) in polymorphonuclear leukocyte (PMN)-induced myocardial ischemia/reperfusion (MI/R) injury and novel-related mechanisms, such as regulation of vascular endothelium nitric oxide (NO) and hydrogen peroxide (H2O2) release from blood vessels, have not been previously evaluated. A cell-permeable PKC epsilon peptide activator (1-10 microM) significantly increased endothelial NO release from non-ischemic rat aortic segments (p < 0.01). By contrast, PKC epsilon peptide inhibitor (1-10 microM) dose-dependently decreased NO release (p < 0.01). Then, these corresponding doses of PKC epsilon activator or inhibitor were examined in MI/R. The PKC epsilon inhibitor (5 microM given during reperfusion, n=6) significantly attenuated PMN-induced postreperfused cardiac contractile dysfunction and PMN adherence/infiltration (both p < 0.01), and expression of intracellular adhesion molecule-1 (ICAM-1; p < 0.05). By contrast, only PKC epsilon activator pretreated hearts (5 muM PKC epsilon activator given before ischemia (PT), n = 6), not PKC epsilon activator given during reperfusion (5 microM, n=6) exerted significant cardioprotection (p < 0.01). Moreover, the NO synthase inhibitor, N(G)-nitro-L: -arginine methyl ester, did not block the cardioprotection of PKC epsilon inhibitor, whereas it completely abolished the cardioprotective effects of PKC epsilon activator PT. In addition, PKC epsilon inhibitor (0.4 mg/kg) significantly decreased H(2)O(2) release during reperfusion in a femoral I/R model (p < 0.01). Therefore, the cardioprotection of PKC epsilon inhibitor maybe related to attenuating ICAM-1 expression and H2O2 release during reperfusion. By contrast, the cardioprotective effects of PKC epsilon activator PT may be mediated by enhancing vascular endothelial NO release before ischemia.

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Protein Kinase C Isoform (PKC) Peptide Activator/Inhibitors Exert Cardioprotective Effects in Polymorphonuclear Leukocyte (PMN)-induced Ischemia/Reperfusion (I/R) Injury

Cited by 2 publications

References 2 publications

Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Mechanisms related to the cardioprotective effects of protein kinase C epsilon (PKC ɛ) peptide activator or inhibitor in rat ischemia/reperfusion injury

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