Protective effects of protein kinase C during myocardial ischemia require activation of phosphatidyl-inositol specific phospholipase C Mamoru Munakata,

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Date of download: 7/9/2016 Copyright © The American College of Cardiology. All rights reserved. From: Fibroblast growth factor-1 improves cardiac functional.

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Protective effects of protein kinase C during myocardial ischemia require activation of phosphatidyl-inositol specific phospholipase C Mamoru Munakata, MD, Christof Stamm, MD, Ingeborg Friehs, MD, David Zurakowski, PhD, Douglas B Cowan, PhD, Hung Cao-Danh, PhD, Francis X McGowan, MD, Pedro J del Nido, MD The Annals of Thoracic Surgery Volume 73, Issue 4, Pages 1236-1245 (April 2002) DOI: 10.1016/S0003-4975(01)03594-9

Fig 1 Phosphatidyl-inositol specific phospholipase C (PI-PLC) activity measured in left ventricular myocardium before (preischemia), after 20 minutes unmodified ischemia at 37°C (end-ischemia), and in hearts treated with the PI-PLC inhibitor U73122 just before ischemia (end-ischemia plus U73122). (Data are mean ± SD; n = 5 per group). Paired t-tests were used to assess changes in PI-PLC activity. The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

Fig 2 Western immunoblots of left ventricular myocardium for protein kinase C (PKC) isoform content. (A) PKC-ε, α, δ, and η content in nonfractionated left ventricular tissue homogenate in nonischemic hearts (control), after 20 minutes of unmodified ischemia (end-ischemia), after preischemic U73122 administration (U73122), and after preischemic administration of U73122 and PMA (U73122 + PMA). Total PKC content was not different between the groups. (B) Subcellular distribution of PKC isoforms assessed in fractionated left ventricular tissue homogenate. (C = cytosolic fraction; P = particulate or membrane fraction. Treatment groups area the same as in A.) (C) Laserdensitometry data demonstrating the translocation pattern of the PKC isoforms (n = 6). Each blot was scanned and the intensity of the respective band was quantified using Scion software. The ratio of PKC isoform in the membranous fraction/PKC isoform in the cytosolic fraction was calculated. The bar graphs represent the mean value ± standard deviation of 6 samples. ∗p < 0.05 versus control by ANOVA. The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

Fig 3 Effect of U73122 dose at the onset of ischemia on postischemic contractile function. (A) Left ventricular developed pressure (expressed as percent of preischemia value) in hearts treated with U73122 for 2.5 minutes just before 20 minutes ischemia at 37°C, followed by 30 minutes of reperfusion. The linear model for predicting developed pressure in % (y) from U73122 dose (x) can be best described by the regression equation: y=−52.5 x+93. (B) Diastolic pressure measured at a fixed balloon volume, after 20 minutes ischemia at 37°C, followed by 30 minutes reperfusion. (Each datum point represents one ischemia-reperfusion experiment.) The linear model for predicting diastolic pressure in mm Hg (y) from U73122 dose (x) can be described by the regression equation: y=43.6 x−2. The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

Fig 4 Postischemic recovery of contractile function. (A) Left ventricular (LV) developed pressure (expressed as percent of the preischemic value) after 20 minutes of ischemia at 37°C, and 30 minutes of reperfusion. (B) Left ventricular diastolic pressure measured at the same balloon volume as preischemia. (C) Rate-pressure product (RPP) LV developed pressure × heart rate, expressed as percent recovery of preischemic RPP). Vehicle or treatment was administered just before the onset of ischemia: control, vehicle (DMSO 0.05%, n = 4); U73343, 0.5 μmol/L U73343 (n = 4); U73122, 0.5 μmol/L U73122 (n = 8); chelerythrine, 2 μmol/L chelerythrine (n = 6); U73122 + PMA, 0.5 μmol/L U73122 plus 10 pmol/L PMA (n = 8). Data are mean ± SD. Groups are compared using ANOVA followed by the Dunnett procedure for multiple comparisons. The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

Fig 4 Postischemic recovery of contractile function. (A) Left ventricular (LV) developed pressure (expressed as percent of the preischemic value) after 20 minutes of ischemia at 37°C, and 30 minutes of reperfusion. (B) Left ventricular diastolic pressure measured at the same balloon volume as preischemia. (C) Rate-pressure product (RPP) LV developed pressure × heart rate, expressed as percent recovery of preischemic RPP). Vehicle or treatment was administered just before the onset of ischemia: control, vehicle (DMSO 0.05%, n = 4); U73343, 0.5 μmol/L U73343 (n = 4); U73122, 0.5 μmol/L U73122 (n = 8); chelerythrine, 2 μmol/L chelerythrine (n = 6); U73122 + PMA, 0.5 μmol/L U73122 plus 10 pmol/L PMA (n = 8). Data are mean ± SD. Groups are compared using ANOVA followed by the Dunnett procedure for multiple comparisons. The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

Fig 5 Effects of U73122 or chelerythrine on contractile function in nonischemic hearts. Left ventricular developed pressure (A) and diastolic pressure (B) after administration of Krebs buffer (control), U73122 (0.5 μmol/L for 2.5 minutes), or chelerythrine (2 μmol/L for 15 minutes). There were no significant differences between control hearts and hearts treated with chelerythrine or U73122 (p > 0.1 each by ANOVA followed by the Dunnett procedure for multiple comparisons). The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)

The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10 The Annals of Thoracic Surgery 2002 73, 1236-1245DOI: (10.1016/S0003-4975(01)03594-9)