Protein Kinase C – Possible Therapeutic Target to Treat Cardiovascular Diseases

2010 ◽  
Vol 10 (4) ◽  
pp. 292-308 ◽  
Author(s):  
Yamini S. Bynagari-Settipalli ◽  
Ramya Chari ◽  
Laurie Kilpatrick ◽  
Satya P. Kunapuli
Keyword(s):  
Protein Kinase C ◽  
Cardiovascular Diseases ◽  
Protein Kinase ◽  
Therapeutic Target ◽  
Kinase C

scholarly journals Effect ofAntrodiacamphorataon Inflammatory Arterial Thrombosis-Mediated Platelet Activation: The Pivotal Role of Protein Kinase C

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Wan-Jung Lu ◽  
Shih-Chang Lin ◽  
Chang-Chou Lan ◽  
Tzu-Yin Lee ◽  
Chih-Hsuan Hsia ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Cardiovascular Diseases ◽  
Protein Kinase ◽  
Platelet Activation ◽  
Vascular Inflammation ◽  
Aortic Aneurysms ◽  
Anticancer Activities ◽  
Antrodia Camphorata ◽  
Intravascular Thrombosis ◽  
Kinase C

Antrodia camphoratais a rare Taiwanese medicinal mushroom.Antrodia camphorataextract has been reported to exhibit antioxidant, anti-inflammation, antimetastasis, and anticancer activities and plays a role in liver fibrosis, vasorelaxation, and immunomodulation. Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Platelet activation plays a crucial role in intravascular thrombosis, which is involved in a wide variety of cardiovascular diseases. However, the effect ofAntrodia camphorataon platelet activation remains unclear. We examined the effects ofAntrodia camphorataon platelet activation. In the present study,Antrodia camphoratatreatment (56–224 μg/mL) inhibited platelet aggregation induced by collagen, but not U46619, an analogue of thromboxane A2, thrombin, and arachidonic acid.Antrodia camphoratainhibited collagen-induced calcium (Ca2+) mobilization and phosphorylation of protein kinase C (PKC) and Akt. In addition,Antrodia camphoratasignificantly reduced the aggregation and phosphorylation of PKC in phorbol-12, 13-dibutyrate (PDBu) activated platelets. In conclusion,Antrodia camphoratamay inhibit platelet activation by inhibiting ofCa2+and PKC cascade and the Akt pathway. Our study suggests thatAntrodia camphoratamay be a potential therapeutic agent for preventing or treating thromboembolic disorders.

scholarly journals Protein Kinase C as a Therapeutic Target

2006 ◽  
Vol 12 (18) ◽  
pp. 5336-5345 ◽  
Author(s):  
Beverly A. Teicher
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Therapeutic Target ◽  
Kinase C

scholarly journals Effects of Sodium Ferulate on Cardiac Hypertrophy Are via the CaSR-Mediated Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Panpan Chen ◽  
Zhaoqin Wen ◽  
Wanlan Shi ◽  
Zhongli Li ◽  
Xiaoyan Chen ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Cardiovascular Diseases ◽  
Protein Kinase ◽  
Cardiac Hypertrophy ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Myocardial Hypertrophy ◽  
Mitogen Activated Protein Kinase ◽  
Kinase C ◽  
Mitogen Activated Protein

As a common complication of many cardiovascular diseases, cardiac hypertrophy is characterized by increased cardiac cell volume, reorganization of the cytoskeleton, and the reactivation of fetal genes such as cardiac natriuretic peptide and β-myosin heavy chain. Cardiac hypertrophy is a distinguishing feature of some cardiovascular diseases. Our previous study showed that sodium ferulate (SF) alleviates myocardial hypertrophy induced by coarctation of the abdominal aorta, and these protective effects may be related to the inhibition of protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) signaling pathways. This study investigated the inhibitory effect and mechanism of SF on myocardial hypertrophy in spontaneously hypertensive rats (SHRs). The effects of SF on cardiac hypertrophy were evaluated using echocardiographic measurement, pathological analysis, and detection of atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC) expression. To investigate the mechanisms underlying the anti-hypertrophic effects of SF, the calcium-sensing receptor (CaSR), calcineurin (CaN), nuclear factor of activated T cells 3 (NFAT3), zinc finger transcription factor 4 (GATA4), protein kinase C beta (PKC-β), Raf-1, extracellular signal-regulated kinase 1/2 (ERK 1/2), and mitogen-activated protein kinase phosphatase-1 (MKP-1) were detected by molecular biology techniques. Treatment with SF ameliorated myocardial hypertrophy in 26-week-old SHRs. In addition, it downregulated the levels of ANP, β-MHC, CaSR, CaN, NFAT3, phosphorylated GATA4 (p-GATA4), PKC-β, Raf-1, and p-ERK 1/2; and upregulated the levels of p-NFAT3 and MKP-1. These results suggest that the effects of SF on cardiac hypertrophy are related to regulation of the CaSR-mediated signaling pathway.

scholarly journals Protein kinase C in heart failure: a therapeutic target?

2008 ◽  
Vol 82 (2) ◽  
pp. 229-239 ◽  
Author(s):  
S. S. Palaniyandi ◽  
L. Sun ◽  
J. C. B. Ferreira ◽  
D. Mochly-Rosen
Keyword(s):  
Heart Failure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Therapeutic Target ◽  
Kinase C

scholarly journals Oxidative Stress in Cardiovascular Diseases and Obesity: Role of p66Shc and Protein Kinase C

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Elena De Marchi ◽  
Federica Baldassari ◽  
Angela Bononi ◽  
Mariusz R. Wieckowski ◽  
Paolo Pinton
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Cardiovascular Diseases ◽  
Protein Kinase ◽  
Cell Signalling ◽  
Redox Balance ◽  
Kinase C ◽  
Antioxidant Defence System ◽  
Normal Metabolism

Reactive oxygen species (ROS) are a byproduct of the normal metabolism of oxygen and have important roles in cell signalling and homeostasis. An imbalance between ROS production and the cellular antioxidant defence system leads to oxidative stress. Environmental factors and genetic interactions play key roles in oxidative stress mediated pathologies. In this paper, we focus on cardiovascular diseases and obesity, disorders strongly related to each other; in which oxidative stress plays a fundamental role. We provide evidence of the key role played byp66Shcprotein and protein kinase C (PKC) in these pathologies by their intracellular regulation of redox balance and oxidative stress levels. Additionally, we discuss possible therapeutic strategies aimed at attenuating the oxidative damage in these diseases.

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