scholarly journals Evidence for Protein Kinase C Dependent Stimulation of Reactive Oxygen Species in Isolated Nuclei of Renal Epithelial Cells

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Bryan Anthony Wilson ◽  
TanYa Gwathmey ◽  
Nancy Pirro ◽  
Mark C Chappell
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Renal Epithelial Cells ◽  
Isolated Nuclei ◽  
Kinase C ◽  
Stimulation Of

Keratin–protein kinase C interaction in reactive oxygen species-induced hepatic cell death through mitochondrial signaling

2008 ◽  
Vol 45 (4) ◽  
pp. 413-424 ◽  
Author(s):  
Jasmin Mathew ◽  
Luc Galarneau ◽  
Anne Loranger ◽  
Stéphane Gilbert ◽  
Normand Marceau
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Reactive Oxygen ◽  
Hepatic Cell ◽  
Oxygen Species ◽  
Kinase C ◽  
Mitochondrial Signaling

scholarly journals Protein Kinase C and PI3 Kinase Mediate Ang II‐Dependent Generation of Reactive Oxygen Species in Renal Nuclei

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Karl D Pendergrass ◽  
TanYa M Gwathmey ◽  
Jason M Grayson ◽  
Mark C Chappell
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Reactive Oxygen ◽  
Pi3 Kinase ◽  
Oxygen Species ◽  
Ang Ii ◽  
Kinase C

The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart

Peptides ◽  
2012 ◽  
Vol 37 (2) ◽  
pp. 314-319 ◽  
Author(s):  
Mahdieh Faghihi ◽  
Ali Mohammad Alizadeh ◽  
Vahid Khori ◽  
Mostafa Latifpour ◽  
Saeed Khodayari
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Heart ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Kinase C

Release of reactive oxygen species by guinea pig tracheal epithelial cells in vitro

1992 ◽  
Vol 262 (6) ◽  
pp. L708-L712 ◽  
Author(s):  
V. L. Kinnula ◽  
K. B. Adler ◽  
N. J. Ackley ◽  
J. D. Crapo
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Guinea Pig ◽  
Oxygen Species ◽  
Tracheal Epithelial Cells ◽  
Kinase C ◽  
Apical Side ◽  
Tracheal Epithelial

Regulatory and stimulatory mechanisms of H2O2 release from guinea pig tracheal epithelial cells were investigated. Cells in primary culture maintained in a previously described air-liquid interface system released H2O2 to the extracellular space only from the apical side of the cells. The rate of release was 0.044 +/- 0.003 nmol.min-1.mg protein-1. H2O2 release could be stimulated significantly during a 30-min incubation period with phorbol myristate acetate (PMA) and platelet-activating factor (PAF). A stimulatory effect of PAF was achieved at concentrations greater than 100 nM and with PMA at concentrations greater than 10 ng (16 nM). When protein kinase C was inactivated with staurosporine, the responses to both PAF and PMA were abolished, whereas the cyclooxygenase inhibitor, indomethacin, did not affect H2O2 generation. When guinea pig tracheal epithelial cells were exposed to sublethal concentrations of extracellular H2O2 (30 microM), H2O2 was detoxified from both apical and basal sides, H2O2 removal being significantly more rapid from the apical side of the cells. These results suggest that tracheal epithelial cells can be stimulated to generate reactive oxygen species into the airway lumen and that this occurs in response to inflammatory mediators that act through protein kinase C. Luminal H2O2 release may have developed as a defense mechanism against microbes, and, similarly, luminal detoxification of H2O2 could represent an important mechanism of modulation of airway inflammation in response to oxidant stress.

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