Ischemic preconditioning promotes a transient, but not sustained translocation of protein kinase C and sensitization of adenylyl cyclase

2003 ◽  
Vol 98 (2) ◽  
pp. 104-113 ◽  
Author(s):  
Gregor Simonis ◽  
Christof Weinbrenner ◽  
Ruth H. Strasser
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adenylyl Cyclase ◽  
Ischemic Preconditioning ◽  
Kinase C

Effects of parathyroid hormone and agonists of the adenylyl cyclase and protein kinase C pathways on bone cell proliferation

Bone ◽  
1996 ◽  
Vol 18 (1) ◽  
pp. 59-65 ◽  
Author(s):  
M. Sabatini ◽  
C. Lesur ◽  
M. Pacherie ◽  
P. Pastoureau ◽  
N. Kucharczyk ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Adenylyl Cyclase ◽  
Bone Cell ◽  
Kinase C ◽  
Bone Cell Proliferation

scholarly journals Disruption of adenylyl cyclase type V does not rescue the phenotype of cardiac-specific overexpression of Gαq protein-induced cardiomyopathy

2010 ◽  
Vol 299 (5) ◽  
pp. H1459-H1467 ◽  
Author(s):  
Valeriy Timofeyev ◽  
Cliff A. Porter ◽  
Dipika Tuteja ◽  
Hong Qiu ◽  
Ning Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Mouse Model ◽  
Transgenic Mice ◽  
Cardiac Function ◽  
Adenylyl Cyclase ◽  
Electrical Remodeling ◽  
Kinase C ◽  
Progressive Heart Failure

Adenylyl cyclase (AC) is the principal effector molecule in the β-adrenergic receptor pathway. ACV and ACVI are the two predominant isoforms in mammalian cardiac myocytes. The disparate roles among AC isoforms in cardiac hypertrophy and progression to heart failure have been under intense investigation. Specifically, the salutary effects resulting from the disruption of ACV have been established in multiple models of cardiomyopathy. It has been proposed that a continual activation of ACV through elevated levels of protein kinase C could play an integral role in mediating a hypertrophic response leading to progressive heart failure. Elevated protein kinase C is a common finding in heart failure and was demonstrated in murine cardiomyopathy from cardiac-specific overexpression of Gαq protein. Here we assessed whether the disruption of ACV expression can improve cardiac function, limit electrophysiological remodeling, or improve survival in the Gαq mouse model of heart failure. We directly tested the effects of gene-targeted disruption of ACV in transgenic mice with cardiac-specific overexpression of Gαq protein using multiple techniques to assess the survival, cardiac function, as well as structural and electrical remodeling. Surprisingly, in contrast to other models of cardiomyopathy, ACV disruption did not improve survival or cardiac function, limit cardiac chamber dilation, halt hypertrophy, or prevent electrical remodeling in Gαq transgenic mice. In conclusion, unlike other established models of cardiomyopathy, disrupting ACV expression in the Gαq mouse model is insufficient to overcome several parallel pathophysiological processes leading to progressive heart failure.

Does Ischemic Preconditioning in the Human Involve Protein Kinase C and the ATP-Dependent K + Channel?

1995 ◽  
Vol 77 (5) ◽  
pp. 1030-1035 ◽  
Author(s):  
M. E. Speechly-Dick ◽  
G. J. Grover ◽  
D. M. Yellon
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
K Channel ◽  
Kinase C

No Prevention of Ischemic Preconditioning by the Protein Kinase C Inhibitor Staurosporine in Swine

1996 ◽  
Vol 79 (3) ◽  
pp. 407-414 ◽  
Author(s):  
Christian Vahlhaus ◽  
Rainer Schulz ◽  
Heiner Post ◽  
Raouf Onallah ◽  
Gerd Heusch
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Kinase C ◽  
Protein Kinase C Inhibitor

Bidirectional modulation of parathyroid hormone-responsive adenylyl cyclase by protein kinase C

1994 ◽  
Vol 266 (6) ◽  
pp. E897-E904 ◽  
Author(s):  
A. M. Kitten ◽  
T. K. Hymer ◽  
M. S. Katz
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Adenylyl Cyclase ◽  
Catalytic Subunit ◽  
Mrna Levels ◽  
Binding Studies ◽  
Kinase C ◽  
Bidirectional Modulation ◽  
Umr 106

The temporal pattern with which phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), modulates parathyroid hormone (PTH)-responsive adenylyl cyclase (AC) was evaluated in a clonal osteoblast-like cell line (UMR-106). Brief (< or = 1 h) exposure of UMR-106 cells to PMA enhanced PTH stimulation of AC, whereas more prolonged PMA treatment decreased the PTH response, with maximum inhibition occurring at < or = 6 h. PMA treatment also resulted in initial activation followed by downregulation of PKC. Exposure of cells to 1,2-dioctanoyl-sn-glycerol, which activated but did not downregulate PKC, resulted in bidirectional modulation of PTH-responsive AC identical to that produced by PMA. Prolonged PMA exposure decreased PTH receptor number, as determined by radioligand binding studies, and reduced PTH receptor mRNA levels, assessed by Northern blot analysis. Forskolin activation of the catalytic subunit of AC was also decreased after prolonged PMA treatment. The results suggest that activation of PKC sequentially stimulates and then inhibits PTH responsiveness. Inhibition of the PTH response occurs by PKC actions exerted on the PTH receptor and the AC catalytic subunit.

scholarly journals Protein kinase C subtypes and retinal ischemic preconditioning

2008 ◽  
Vol 87 (4) ◽  
pp. 300-311 ◽  
Author(s):  
John C. Dreixler ◽  
Afzhal R. Shaikh ◽  
Shanti K. Shenoy ◽  
Yang Shen ◽  
Steven Roth
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Kinase C

Roles of Tyrosine Kinase and Protein Kinase C in Infarct Size Limitation by Repetitive Ischemic Preconditioning in the Rat

2000 ◽  
Vol 35 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Masaya Tanno ◽  
Akihito Tsuchida ◽  
Yukinaga Nozawa ◽  
Tomoaki Matsumoto ◽  
Tohru Hasegawa ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Kinase C ◽  
Size Limitation ◽  
Infarct Size Limitation
Sign in / Sign up

Export Citation Format

Share Document