Protection by 6-aminonicotinamide against oxidative stress in cardiac cells

Hofgaard, Johannes P.; Sigurdardottir, Kristin Sigridur; Treiman, Marek

doi:10.1016/j.phrs.2006.06.007

Cited by 10 publications

(4 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To date, several studies, mostly on preconditioning, identified many PKCε target proteins that may play a role in cardioprotection. It has been demonstrated that PKCε-mediated cardioprotection is linked to phosphorylation of connexin 43 (Doble et al 2000, Jeyaraman et al 2012, which among the other effects influences the gap junctional intercellular communication and thereby may prevent the spreading of injury during I/R. PKCε also activates aldehyde dehydrogenase-2, which metabolizes toxic aldehydes formed during I/R (Budas et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Having considered the effective concentrations of the KP-1633 resembling peptide εV1-2 used in other studies (Chen et al 1999), the concentrations of 0.1, 1, 5, 10 and 50 μM KP-1633 and KP-1723 were tested. The percentage of living cells compared to the untreated control cells was assessed with SYTOX Green nucleic acid stain (S7020) (Invitrogen-Molecular Probes, Eugene, OR, USA) at the beginning of the experiment (after stabilization) and after 2, 4 and 20 h. The fluorescence signal of SYTOX Green, which is proportional to the number of dead cells (Hofgaard et al 2006), was measured at an excitation wavelength of 490 nm and emission wavelength of 520 nm using a Synergy™ HT Multi-Detection Microplate Reader (BioTek, Winooski, VT, USA). Decreasing viability of LVM was already observed after 4-h incubation with 10 μM KP-1633 and after 2, 4 and 20-h incubation with 50 μM KP-1723 (data not shown).…”

Section: Assessment Of Cell Viability With Sytox Greenmentioning

confidence: 99%

See 1 more Smart Citation

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Holzerová

Hlaváčková

Žurmanová³

et al. 2015

Physiol Res

View full text Add to dashboard Cite

Continuous normobaric hypoxia (CNH) renders the heart more tolerant to acute ischemia/reperfusion injury. Protein kinase C (PKC) is an important component of the protective signaling pathway, but the contribution of individual PKC isoforms under different hypoxic conditions is poorly understood. The aim of this study was to analyze the expression of PKCε after the adaptation to CNH and to clarify its role in increased cardiac ischemic tolerance with the use of PKCε inhibitory peptide KP-1633. Adult male Wistar rats were exposed to CNH (10 % O2, 3 weeks) or kept under normoxic conditions. The protein level of PKCε and its phosphorylated form was analyzed by Western blot in homogenate, cytosolic and particulate fractions; the expression of PKCε mRNA was measured by RT-PCR. The effect of KP-1633 on cell viability and lactate dehydrogenase (LDH) release was analyzed after 25-min metabolic inhibition followed by 30-min re-energization in freshly isolated left ventricular myocytes. Adaptation to CNH increased myocardial PKCε at protein and mRNA levels. The application of KP-1633 blunted the hypoxia-induced salutary effects on cell viability and LDH release, while control peptide KP-1723 had no effect. This study indicates that PKCε is involved in the cardioprotective mechanism induced by CNH.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Assessment Of Cell Viability With Sytox Greenmentioning

confidence: 99%

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Holzerová

Hlaváčková

Žurmanová³

et al. 2015

Physiol Res

View full text Add to dashboard Cite

show abstract

“…The fluorescence signal of SYTOX green is proportional to the number of dead cells. 23 At the end of the experiments, all cells were lysed with 1% triton X100 to get the signal for 100% dead cells. From this number, the signal observed before lysis was subtracted to obtain the percentage of surviving cells for each group.…”

Section: Methodsmentioning

confidence: 99%

Pharmacological activation of mitochondrial BK_Ca channels protects isolated cardiomyocytes against simulated reperfusion-induced injury

Borchert

Hlaváčková

Kolář

2013

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

The aim of this study was to find out whether opening of mitochondrial large-conductance Ca(2+)-activated potassium channels (BK(Ca)) protects cardiomyocytes against injury caused by simulated ischemia and reperfusion. This study also aimed to determine whether the protective mechanism involves signaling by reactive oxygen species (ROS) and phosphatidylinositol-3-kinase (PI3K). We used isolated ventricular myocytes, which are believed to contain no functional BK(Ca) channels in the sarcolemma. Cells were isolated from the left ventricles of adult male Wistar rats and subjected to 25-min metabolic inhibition with NaCN and 2-deoxyglucose followed by 30-min re-energization. NS11021 (0.1 μmol/L), a novel BK(Ca) channel opener, or hydrogen peroxide (2 μmol/L) added at re-energization, increased cell survival (the number of rod-shaped cells) and markedly reduced the release of lactate dehydrogenase (LDH). These cytoprotective effects of NS11021 were completely abolished by paxilline, a BK(Ca) inhibitor, or tempol, an antioxidant, but not by wortmannin, an inhibitor of PI3K. NS11021 slightly but significantly increased the fluorescence signal in 2'7'-dichlorodihydrofluorescein diacetate (DCF-DA)-loaded myocytes, indicating an increased ROS formation. The NS11021-induced ROS formation was abolished by paxilline or tempol. NS13558 (0.1 μmol/L), an inactive structural analogue of NS11021, affected neither cell survival/LDH release nor DCF-DA fluorescence. These results suggest that pharmacological activation of mitochondrial BK(Ca) channels effectively protects isolated cardiomyocytes against injury associated with simulated reperfusion. The mechanism for this form of protection requires ROS signaling, but not the activation of the PI3K pathway.

show abstract

“…Oxidative 207 stress has been previously modeled in the freshly isolated cardiomyocytes of Wistar newborn 208 rats with hydrogen peroxide (H 2 O 2 ), which alters the [Ca 2+ ] i in the concentration range of 10 -2 -209 10 -8 M(Hofgaard, Sigurdardottir, & Treiman, 2006). The cardiomyocytes were isolated as 210 described earlier(Belostotskaya & Golovanova, 2014).…”

mentioning

confidence: 99%

Modified hydroxyethyl starch protects cells from oxidative damage

Filippov

Sergeeva

Vlasov

et al. 2015

Carbohydrate Polymers

View full text Add to dashboard Cite

Protection by 6-aminonicotinamide against oxidative stress in cardiac cells

Cited by 10 publications

References 44 publications

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Pharmacological activation of mitochondrial BK_Ca channels protects isolated cardiomyocytes against simulated reperfusion-induced injury

Modified hydroxyethyl starch protects cells from oxidative damage

Contact Info

Product

Resources

About

Protection by 6-aminonicotinamide against oxidative stress in cardiac cells

Cited by 10 publications

References 44 publications

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Involvement of PKCε in Cardioprotection Induced by Adaptation to Chronic Continuous Hypoxia

Pharmacological activation of mitochondrial BKCa channels protects isolated cardiomyocytes against simulated reperfusion-induced injury

Modified hydroxyethyl starch protects cells from oxidative damage

Contact Info

Product

Resources

About

Pharmacological activation of mitochondrial BK_Ca channels protects isolated cardiomyocytes against simulated reperfusion-induced injury