scholarly journals Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia

2018 ◽  
Vol 37 (05) ◽  
pp. 537-547
Author(s):  
S. Y. Tsibulnikov ◽  
L. N. Maslov ◽  
N. V. Naryzhnaya ◽  
H. Ma ◽  
Y. B. Lishmanov ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Tyrosine Kinases ◽  
Katp Channels ◽  
No Synthase ◽  
Pi3 Kinase ◽  
Cardioprotective Effect ◽  
Kinase C

Opioid Peptide Deltorphin II Simulates the Cardioprotective Effect of Ischemic Preconditioning: Role of δ2-Opioid Receptors, Protein Kinase C, and KATP Channels

2010 ◽  
Vol 149 (5) ◽  
pp. 591-593 ◽  
Author(s):  
L. N. Maslov ◽  
E. I. Barzakh ◽  
A. V. Krylatov ◽  
G. A. Chernysheva ◽  
T. Krieg ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptors ◽  
Ischemic Preconditioning ◽  
Katp Channels ◽  
Opioid Peptide ◽  
Cardioprotective Effect ◽  
Kinase C ◽  
Deltorphin Ii

Role of the protein kinase C signaling pathway in the regulation of claudin-4 in normal human pancreatic duct epithelial cells and cancer cells

Pancreatology ◽  
2012 ◽  
Vol 12 (6) ◽  
pp. 584-585
Author(s):  
H. Yamaguchi ◽  
T. Kojima ◽  
D. Kyuno ◽  
T. Ito ◽  
Y. Kimura ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Pancreatic Duct ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Kinase C ◽  
Normal Human

Role of Tyrosine Kinases, Protein Kinase C, and Protein Kinase A in the Regulation of Interferon-α Production Induced by Herpes Simplex Virus Type 1

1996 ◽  
Vol 16 (2) ◽  
pp. 109-118 ◽  
Author(s):  
QUANHUI LI ◽  
MICHAEL FELDMAN ◽  
CAROLYN HARMON ◽  
PATRICIA FITZGERALD-BOCARSLY
Keyword(s):  
Protein Kinase C ◽  
Herpes Simplex ◽  
Protein Kinase ◽  
Tyrosine Kinases ◽  
Interferon Α ◽  
Kinase C ◽  
Simplex Virus ◽  
Kinase A

The Cardioprotective Effect of Ischemic Preconditioning : Role of Adenosine and Protein Kinase C

1997 ◽  
Vol 27 (10) ◽  
pp. 1004
Author(s):  
Hyun Kim ◽  
Dae-Joong Kim ◽  
Sung-Soo Kim ◽  
Bong-Jin Rah ◽  
Ho-Dirk Kim
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Cardioprotective Effect ◽  
Kinase C

Platelet-activating factor induces cardioprotection in isolated rat heart akin to ischemic preconditioning: role of phosphoinositide 3-kinase and protein kinase C activation

2005 ◽  
Vol 288 (5) ◽  
pp. H2512-H2520 ◽  
Author(s):  
Claudia Penna ◽  
Giuseppe Alloatti ◽  
Sandra Cappello ◽  
Donatella Gattullo ◽  
Giovanni Berta ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Platelet Activating Factor ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Cardioprotective Effect ◽  
Kinase C ◽  
Phosphoinositide 3 Kinase

Ischemic preconditioning (IP) is a cardioprotective mechanism against myocellular death and cardiac dysfunction resulting from reperfusion of the ischemic heart. At present, the precise list of mediators involved in IP and the pathways of their mechanisms of action are not completely known. The aim of the present study was to investigate the role of platelet-activating factor (PAF), a phospholipid mediator that is known to be released by the ischemic-reperfused heart, as a possible endogenous agent involved in IP. Experiments were performed on Langendorff-perfused rat hearts undergoing 30 min of ischemia followed by 2 h of reperfusion. Treatment with a low concentration of PAF (2 × 10−11 M) before ischemia reduced the extension of infarct size and improved the recovery of left ventricular developed pressure during reperfusion. The cardioprotective effect of PAF was comparable to that observed in hearts in which IP was induced by three brief (3 min) periods of ischemia separated by 5-min reperfusion intervals. The PAF receptor antagonist WEB-2170 (1 × 10−9 M) abrogated the cardioprotective effect induced by both PAF and IP. The protein kinase C (PKC) inhibitor chelerythrine (5 × 10−6 M) or the phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 (5 × 10−5 M) also reduced the cardioprotective effect of PAF. Western blot analysis revealed that following IP treatment or PAF infusion, the phosphorylation of PKC-ε and Akt (the downstream target of PI3K) was higher than that in control hearts. The present data indicate that exogenous applications of low quantities of PAF induce a cardioprotective effect through PI3K and PKC activation, similar to that afforded by IP. Moreover, the study suggests that endogenous release of PAF, induced by brief periods of ischemia and reperfusion, may participate to the triggering of the IP of the heart.

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 Potentiation of Protein Kinase C ζ Activity by 15-Deoxy-Δ12,14-Prostaglandin J2 Induces an Imbalance between Mitogen-Activated Protein Kinases and NF-κB That Promotes Apoptosis in Macrophages

2003 ◽  
Vol 23 (4) ◽  
pp. 1196-1208 ◽  
Author(s):  
Antonio Castrillo ◽  
Paqui G. Través ◽  
Paloma Martín-Sanz ◽  
Scott Parkinson ◽  
Peter J. Parker ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Direct Action ◽  
Pi3 Kinase ◽  
Activated Macrophages ◽  
Kinase C ◽  
Iκb Kinase ◽  
Mitogen Activated Protein ◽  
Sustained Activation

ABSTRACT Activation of the macrophage cell line RAW 264.7 with lipopolysaccharide (LPS) transiently activates protein kinase C ζ (PKCζ) and Jun N-terminal kinase (JNK) through a phosphoinositide-3-kinase (PI3-kinase)-dependent pathway. Incubation of LPS-treated cells with the cyclopentenone 15-deoxy-Δ12,14-prostaglandin J2 (15dPGJ2) promoted a sustained activation of PKCζ and JNK and inhibited IκB kinase (IKK) and NF-κB activity. Accordingly, 15dPGJ2 induced an imbalance between JNK and IKK activities by increasing the former signaling pathway and inhibiting the latter signaling pathway. Under these conditions, apoptosis was significantly enhanced; this response was very dependent on PKCζ and JNK activation. The effect of 15dPGJ2 on PKCζ activity observed in LPS-activated macrophages was not dependent on a direct action of this prostaglandin on the enzyme but was due to the activation of a step upstream of PI3-kinase. Moreover, LPS promoted the redistribution of activated PKCζ from the cytosol to the nucleus, a process that was enhanced by treatment of the cells with 15dPGJ2 that favored a persistent and broader distribution of PKCζ in the nucleus. These results indicate that 15dPGJ2 and other cyclopentenone prostaglandins, through the sustained activation of PKCζ, might contribute significantly to the process of resolution of inflammation by promoting apoptosis of activated macrophages.

Activation of k1-opioid receptor as a method for prevention of ischemic and reperfusion arrhythmias: Role of protein kinase C and KATP channels

2007 ◽  
Vol 143 (2) ◽  
pp. 187-190 ◽  
Author(s):  
A. Yu. Lishmanov ◽  
L. N. Maslov ◽  
T. V. Lasukova ◽  
D. Crawford ◽  
T. M. Wong
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptor ◽  
Katp Channels ◽  
Reperfusion Arrhythmias ◽  
Kinase C
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