Arachidonic acid protects neonatal rat cardiac myocytes from ischaemic injury through ε protein kinase C

Mackay, Katrina; Mochly‐Rosen, Daria

doi:10.1016/s0008-6363(00)00322-9

Cited by 56 publications

(32 citation statements)

References 59 publications

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“…18) Briefly, the rat ventricular myocardium was surgically removed, minced into 1-3 mm 3 pieces, and then washed twice in phosphate-buffered saline (PBS). The minced tissues were dissociated by 4-6 repeated exposures to 0.25% (wt/vol) trypsin/1 mM EDTA solution at 37°C, along with gentle agitation.…”

Section: Methodsmentioning

confidence: 99%

Taurine Protects Primary Neonatal Cardiomyocytes Against Apoptosis Induced by Hydrogen Peroxide

Wang

Liu

et al. 2018

Int. Heart J.

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SummaryThe aim of this study was to investigate the effects of taurine (Tau) on primary cultured neonatal myocardial cells treated with hydrogen peroxide (H2O2) and the underlying mechanism. Primary cardiac myocytes from neonatal Wistar rats were pre-incubated with Tau, and its effects on cell viability and expression of CaM, CaM-KII, p53, Bcl-2, and Bax were examined. Tau enhanced the viability of myocardial cells, decreased apoptosis, and alleviated the intracellular calcium overload, especially at dosages of 40 or 80 mM (P < 0.01 or P < 0.001, respectively). Moreover, Tau could inhibit the H2O2-induced decrease in CamKII and CaM expression at both the mRNA and protein levels. The pattern of CaMKII expression was consistent with that of the anti-apoptotic protein Bcl-2, but contrasted the pattern of the pro-apoptotic proteins p53 and Bax. Thus, our results show that Tau protects myocardial cells against damage caused by H2O2 exposure, suggesting that it might play a role in the mitochondrial apoptotic pathway by upregulating the expression of CaMKII to rescue myocardial cells. However, the underlying mechanism still needs to be investigated. In addition, we tested the protective effect of taurine on cardiac myocytes, and the effect of taurine on another model, specifically an animal model. (Int Heart J 2018; 59: 190-196)

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Section: Methodsmentioning

confidence: 99%

Taurine Protects Primary Neonatal Cardiomyocytes Against Apoptosis Induced by Hydrogen Peroxide

Wang

Liu

et al. 2018

Int. Heart J.

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“…This method is adapted from one described previously (Mackay and Mochly-Rosen, 2001). Hippocampal organotypic slices were frozen in liquid nitrogen at different time intervals and stored at Ϫ80°C until the analysis.…”

Section: Cell Fractionation and Western Blot Analysismentioning

confidence: 99%

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

et al. 2003

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Glutamate receptors and calcium have been implicated as triggering factors in the induction of tolerance by ischemic preconditioning (IPC) in the brain. However, little is known about the signal transduction pathway that ensues after the IPC induction pathway. The main goals of the present study were to determine whether NMDA induces preconditioning via a calcium pathway and promotes translocation of the protein kinase C ⑀ (⑀PKC) isozyme and whether this PKC isozyme is key in the IPC signal transduction pathway. We corroborate here that IPC and a sublethal dose of NMDA were neuroprotective, whereas blockade of NMDA receptors during IPC diminished IPC-induced neuroprotection. Calcium chelation blocked the protection afforded by both NMDA and ischemic preconditioning significantly, suggesting a significant role of calcium. Pharmacological preconditioning with the nonselective PKC isozyme activator phorbol myristate acetate could not emulate IPC, but blockade of PKC activation with chelerythrine during IPC blocked its neuroprotection. These results suggested that there might be a dual involvement of PKC isozymes during IPC. This was corroborated when neuroprotection was blocked when we inhibited ⑀PKC during IPC and NMDA preconditioning, and IPC neuroprotection was emulated with the activator of ⑀PKC. The possible correlation between NMDA, Ca 2ϩ , and ⑀PKC was found when we emulated IPC with the diacylglycerol analog oleoylacetyl glycerol, suggesting an indirect pathway by which Ca 2ϩ could activate the calcium-insensitive ⑀PKC isozyme. These results demonstrated that the ⑀PKC isozyme played a key role in both IPC-and NMDA-induced tolerance.

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“…Western blot analysis was also performed on organotypic slices at 3 h following OGD and/or after various inhibitor treatments as described previously (Mackay and Mochly-Rosen, 2001;Raval et al, 2003). Hippocampal organotypic slices were frozen in liquid nitrogen and stored at À801C until the analysis.…”

Section: Cell Fractionation and Western Blot Analysismentioning

confidence: 99%

Protein Kinase C Delta Cleavage Initiates an Aberrant Signal Transduction Pathway after Cardiac Arrest and Oxygen Glucose Deprivation

Raval

Dave

Prado

et al. 2005

J Cereb Blood Flow Metab

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Protein kinase C (PKC) isozymes have been known to mediate a variety of complex and diverse cellular functions. dPKC has been implicated in mediating apoptosis. Using two models of cerebral ischemia, cardiac arrest in rats and oxygen glucose deprivation (OGD) in organotypic hippocampal slices, we tested whether an ischemic insult promoted dPKC cleavage during the reperfusion and whether the upstream pathway involved release of cytochrome c and caspase 3 cleavage. We showed that cardiac arrest/OGD significantly enhanced dPKC translocation and increased its cleavage at 3 h of reperfusion. Since dPKC is one of the substrates for caspase 3, we next determined caspase 3 activation after cardiac arrest and OGD. The maximum decrease in levels of procaspase 3 was observed at 3 h of reperfusion after cardiac arrest and OGD. We also determined cytochrome c release, since it is upstream of caspase 3 activation. Cytochrome c in cytosol increased at 1 h of reperfusion after cardiac arrest/OGD. Inhibition of either dPKC/caspase 3 during OGD and early reperfusion resulted in neuroprotection in CA1 region of hippocampus. Our results support the deleterious role of dPKC in reperfusion injury. We propose that early cytochrome c release and caspase 3 activation promote dPKC translocation/cleavage.

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Arachidonic acid protects neonatal rat cardiac myocytes from ischaemic injury through ε protein kinase C

Cited by 56 publications

References 59 publications

Taurine Protects Primary Neonatal Cardiomyocytes Against Apoptosis Induced by Hydrogen Peroxide

Taurine Protects Primary Neonatal Cardiomyocytes Against Apoptosis Induced by Hydrogen Peroxide

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

Protein Kinase C Delta Cleavage Initiates an Aberrant Signal Transduction Pathway after Cardiac Arrest and Oxygen Glucose Deprivation

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