The role of protein kinase C beta 2 (PKC β2) in myocardial ischaemia-reperfusion injury

2014 ◽  
Author(s):  
Jiqin Jin
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischaemia Reperfusion Injury ◽  
Kinase C ◽  
Ischaemia Reperfusion ◽  
Beta 2 ◽  
Protein Kinase C Beta

Abstract 447: Myristoylation of Protein Kinase C Beta II Peptide Inhibitor Facilitates Rapid Attenuation of Phorbol 12-myristate 13-acetate in Activated Superoxide Release in Isolated Rat Polymorphonuclear Leukocytes

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Sunit G Singh ◽  
Tameka Dean ◽  
Michael Lloyd ◽  
Rourke Decker ◽  
Jeremy Castro ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemia Reperfusion ◽  
Peptide Inhibitor ◽  
Trypan Blue Exclusion ◽  
Kinase C ◽  
Myocardial Ischemia Reperfusion ◽  
Post Hoc ◽  
Protein Kinase C Beta

Protein kinase C beta II (PKCβII) activates polymorphonuclear leukocyte (PMN) superoxide (SO) production via NADPH oxidase (NOX-2) phosphorylation to exacerbate myocardial ischemia/reperfusion (I/R) injury. In prior studies, myristoylation (myr) of PKCβII peptide inhibitor (N-myr-SLNPEWNET; myr-PKCβII-), which disrupts PKCβII translocation/phosphorylation of NOX-2, was shown to dose-dependently attenuate PMN SO release induced by phorbol 12-myristate 13-acetate (PMA), a broad-spectrum PKC agonist. However, the role of myr on the inhibitory effects of myr-PKCβII- has yet to be elucidated. We hypothesized that myr-PKCβII peptide activator (N-myr-SVEIWD; myr-PKCβII+) would augment, myr-PKCβII- would attenuate, and scrambled myr-PKCβII- (N-myr-WNPESLNTE; myr-PKCβII-scram), a control for myr, would not affect PMA-induced PMN SO release compared to unconjugated peptides and nontreated controls. Rat PMNs (5х10 6 ) were incubated for 15 min at 37 o C in the presence/absence of SO dismutase (SOD; 10 μg/mL), unconjugated PKCβII+/-, myr-PKCβII+/-, or myr-PKCβII-scram (all 20 μM). SO release was measured by the change in absorbance at 550 nm via ferricytochrome c reduction after PMA (100 nM) stimulation for 390 sec. Data were analyzed by ANOVA using Student-Newman-Keuls post hoc analysis. Myr-PKCβII- significantly attenuated SO release (0.30±0.02; n=27; p<0.05) compared to nontreated controls (0.46±0.01; n=73), myr-PKCβII+ (0.46±0.03; n=25), unconjugated PKCβII+ (0.43±0.04; n=15), PKCβII- (0.43±0.02; n=22) and myr-PKCβII-scram (0.65±0.04; n=22). SOD (n=8), which rapidly converts SO to H 2 O 2 , significantly reduced absorbance by 94±7%, indicating that absorbance increased mainly due to PMA stimulation. Cell viability (trypan blue exclusion) was similar in all groups (94±2%). Unexpectedly, myr-PKCβII-scram significantly stimulated the highest increase in absorbance compared to all groups (p<0.01). Future studies will determine whether myr-PKCβII-scram augments absorbance by a different mechanism. Results suggest that myr improves myr-PKCβII- delivery compared to unconjugated PKCβII- but does not affect inhibition of PMA-induced PMN SO release. Myr-PKCβII- may thus effectively limit inflammation-induced I/R injury.

scholarly journals BS31 The role of fractalkine and CX3CR1-expressing lymphocytes during myocardial ischaemia/reperfusion injury

2019 ◽  
Author(s):  
Lilia Draganova ◽  
Rachael Redgrave ◽  
Simon Tual-Chalot ◽  
Sarah Marsh ◽  
Helen Arthur ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals Sildenafil-mediated neovascularization and protection against myocardial ischaemia reperfusion injury in rats: role of VEGF/angiopoietin-1

2008 ◽  
Vol 12 (6b) ◽  
pp. 2651-2664 ◽  
Author(s):  
Srikanth Koneru ◽  
Suresh Varma Penumathsa ◽  
Mahesh Thirunavukkarasu ◽  
Ramesh Vidavalur ◽  
Lijun Zhan ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Angiopoietin 1
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