scholarly journals The role of protein kinase C and PI3-kinase in the mechanism of the cardioprotective effect of remote ischemic postconditioning

2022 ◽  
Vol 20 (4) ◽  
pp. 6-10
Author(s):  
A. V. Mukhomedzyanov ◽  
N. V. Naryzhnaya ◽  
L. N. Maslov
Keyword(s):  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Coronary Blood Flow ◽  
Pi3 Kinase ◽  
Ischemic Postconditioning ◽  
Kinase C ◽  
Remote Ischemic Postconditioning

Background. Acute myocardial infarction (AMI) with ST segment elevation is associated with high incidence of complications. Mortality from AMI is about 5%, which has not decreased in recent years. Revascularization provides recovery of coronary blood flow, but also contributes to the occurrence of reperfusion injury to the heart. Remote ischemic postconditioning (RIPostC) is a promising, non-invasive method that can effectively and safely reduce the infarct size.The aim of the study was to investigate the role of protein kinase C and PI3-kinase in the development of the infarct-limiting effect of remote ischemic postconditioning.Materials and methods. The study was performed on Wistar rats. Coronary artery occlusion (45 min) and reperfusion (2 h) were performed. The infarct size (IS) and the size of area at risk (AAR) were assessed. RIPostC was modeled by applying tourniquets to the hind limbs in the hip joint immediately after the restoration of coronary blood flow. All inhibitors were administered intravenously 10 min before reperfusion.Results. In the control group, the IS / AAR ratio was 44%. RIPostC reduced the IS / AAR ratio by about 50%. Preliminary administration of the protein kinase C inhibitor chelerythrine and the PI3-kinase inhibitor wortmannin eliminated the cardioprotective effect of RIPostC.Conclusion. The mechanism of the infarct-limiting effect of RIPostC is implemented through activation of protein kinase C and PI3-kinase. 

scholarly journals Erratum

1992 ◽  
Vol 12 (4) ◽  
pp. 707-707 ◽  
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Protein Kinase C ◽  
Cerebral Blood Flow ◽  
Protein Kinase ◽  
Vertical Axis ◽  
Smooth Muscle Contraction ◽  
Kinase C ◽  
Chronic Cerebral Vasospasm

Possible Role of Protein Kinase C-Dependent Smooth Muscle Contraction in the Pathogenesis of Chronic Cerebral Vasospasm Tohru Matsui, Yoh Takuwa, Hiroo Johshita, Kamejiro Yamashita, and Takao Asano [Originally published in Journal of Cerebral Blood Flow and Metabolism 1992;11:143–149] On page 147 of the above, the unit on the left vertical axis of Figure 3 was incorrectly shown as “DAG Level (fLmollmg . protein).” The correct unit is “nmollmg protein.” The figure is shown below. The authors regret this error. [Figure: see text]

Novel functional role of heat shock protein 90 in protein kinase C-mediated ischemic postconditioning

2014 ◽  
Vol 189 (2) ◽  
pp. 198-206 ◽  
Author(s):  
Guo-Qiang Zhong ◽  
Rong-Hui Tu ◽  
Zhi-Yu Zeng ◽  
Qing-jie Li ◽  
Yan He ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Heat Shock ◽  
Protein Kinase ◽  
Heat Shock Protein ◽  
Functional Role ◽  
Heat Shock Protein 90 ◽  
Ischemic Postconditioning ◽  
Kinase C

Protein kinase C plays an essential role in sildenafil-induced cardioprotection in rabbits

2004 ◽  
Vol 286 (4) ◽  
pp. H1455-H1460 ◽  
Author(s):  
Anindita Das ◽  
Ramzi Ockaili ◽  
Fadi Salloum ◽  
Rakesh C. Kukreja
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Essential Role ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sildenafil Citrate ◽  
Risk Area ◽  
Kinase C

Sildenafil citrate (Viagra) is the most widely used pharmacological drug for treating erectile dysfunction in men. It has potent cardioprotective effects against ischemia-reperfusion injury via nitric oxide and opening of mitochondrial ATP-sensitive K+ channels. We further investigated the role of protein kinase C (PKC)-dependent signaling pathway in sildenafil-induced cardioprotection. Rabbits were treated (orally) with sildenafil citrate (1.4 mg/kg) 30 min before index ischemia for 30 min and reperfusion for 3 h. The PKC inhibitor chelerythrine (5 mg/kg iv) was given 5 min before sildenafil. Infarct size (% of risk area) reduced from 33.65 ± 2.17 in the vehicle (saline) group to 15.07 ± 0.63 in sildenafil-treated groups, a 45% reduction compared with vehicle (mean ± SE, P < 0.05). Chelerythrine abolished sildenafil-induced protection, as demonstrated by increase in infarct size to 31.14 ± 2.4 ( P < 0.05). Chelerythrine alone had an infarct size of 33.5 ± 2.5, which was not significantly different compared with DMSO-treated group (36.8 ± 1.7, P > 0.05). Western blot analysis demonstrated translocation of PKC-α, -θ, and -δ isoforms from cytosol to membrane after treatment with sildenafil. However, no change in the PKC-β and -ϵ isoforms was observed. These data provide direct evidence of an essential role of PKC, and potentially PKC-α, -θ, and -δ, in sildenafil-induced cardioprotection in the rabbit heart.

scholarly journals Role of protein kinase C in the reduction of infarct size by N -methyl-1-deoxynojirimycin, an α-1,6-glucosidase inhibitor

2001 ◽  
Vol 133 (5) ◽  
pp. 635-642 ◽  
Author(s):  
Masazumi Arai ◽  
Shinya Minatoguchi ◽  
Hirokazu Kumada ◽  
Yoshihiro Uno ◽  
Yoshio Nishida ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Glucosidase Inhibitor ◽  
Kinase C

Role of protein kinase C in the regulation of steroidogenesis in the mouse Leydig cell

1986 ◽  
Vol 113 (1_Suppl) ◽  
pp. S63-S64
Author(s):  
A. K. MUKHOPADHYAY ◽  
H. G. BOHNET
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Leydig Cell ◽  
Kinase C ◽  
Mouse Leydig Cell

scholarly journals Dysregulation of protein kinase C in adult depression and suicide: evidence from postmortem brain studies

2021 ◽  
Author(s):  
Ghanshyam N Pandey ◽  
Anuradha Sharma ◽  
Hooriyah S Rizavi ◽  
Xinguo Ren
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Expression ◽  
Mrna Expression ◽  
Postmortem Brain ◽  
Cortical Region ◽  
Cytosol Fraction ◽  
Kinase C ◽  
Pkc Isozymes

Abstract Background Several lines of evidence suggest the abnormalities of protein kinase C (PKC) signaling system in mood disorders and suicide based primarily on the studies of PKC and its isozymes in the platelets and postmortem brain of depressed and suicidal subjects. In this study we examined the role of PKC isozymes in depression and suicide. Methods We determined the protein and mRNA expression of various PKC isozymes in the prefrontal cortical region [Brodmann area 9 (BA9)] in 24 normal control (NC) subjects, 24 depressed suicide (DS) subjects and 12 depressed non-suicide (DNS) subjects. The levels of mRNA in the prefrontal cortex (PFC) were determined by qRT-PCR and the protein expression was determined by Western blotting. Results We observed a significant decrease in mRNA expression of PKCα, PKCβI, PKCδ and PKCε and decreased protein expression either in the membrane or the cytosol fraction of PKC isozymes - PKCα, PKCβI, PKCβII and PKCδ in DS and DNS subjects compared with NC subjects. Conclusions The current study provides detailed evidence of specific dysregulation of certain PKC isozymes in the postmortem brain of DS and DNS subjects and further supports earlier evidence for the role of PKC in the platelets and brain of adult and teenage depressed and suicidal population. This comprehensive study may lead to further knowledge of the involvement of PKC in the pathophysiology of depression and suicide.

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