scholarly journals Protein Kinase A Anchoring via AKAP150 Is Essential for TRPV1 Modulation by Forskolin and Prostaglandin E2 in Mouse Sensory Neurons

2008 ◽  
Vol 28 (19) ◽  
pp. 4904-4917 ◽  
Author(s):  
K. Schnizler ◽  
L. P. Shutov ◽  
M. J. Van Kanegan ◽  
M. A. Merrill ◽  
B. Nichols ◽  
...  
2002 ◽  
Vol 215 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Michael M Hayes ◽  
Brian R Lane ◽  
Steven R King ◽  
David M Markovitz ◽  
Michael J Coffey

Blood ◽  
2012 ◽  
Vol 119 (10) ◽  
pp. 2358-2367 ◽  
Author(s):  
Zbigniew Zasłona ◽  
Carlos H. Serezani ◽  
Katsuhide Okunishi ◽  
David M. Aronoff ◽  
Marc Peters-Golden

Abstract Prostaglandin E2 (PGE2) is a lipid mediator that acts by ligating 4 distinct G protein–coupled receptors, E prostanoid (EP) 1 to 4. Previous studies identified the importance of PGE2 in regulating macrophage functions, but little is known about its effect on macrophage maturation. Macrophage maturation was studied in vitro in bone marrow cell cultures, and in vivo in a model of peritonitis. EP2 was the most abundant PGE2 receptor expressed by bone marrow cells, and its expression further increased during macrophage maturation. EP2-deficient (EP2−/−) macrophages exhibited enhanced in vitro maturation compared with wild-type cells, as evidenced by higher F4/80 expression. An EP2 antagonist also increased maturation. In the peritonitis model, EP2−/− mice exhibited a higher percentage of F4/80high/CD11bhigh cells and greater expression of macrophage colony-stimulating factor receptor (M-CSFR) in both the blood and the peritoneal cavity. Subcutaneous injection of the PGE2 analog misoprostol decreased M-CSFR expression in bone marrow cells and reduced the number of peritoneal macrophages in wild-type mice but not EP2−/− mice. The suppressive effect of EP2 ligation on in vitro macrophage maturation was mimicked by a selective protein kinase A agonist. Our findings reveal a novel role for PGE2/EP2/protein kinase A signaling in the suppression of macrophage maturation.


2006 ◽  
Vol 5 (7) ◽  
pp. 1817-1826 ◽  
Author(s):  
Troy Payner ◽  
H. Anne Leaver ◽  
Brian Knapp ◽  
Ian R. Whittle ◽  
Ovidiu C. Trifan ◽  
...  

1991 ◽  
Vol 49 (1) ◽  
pp. 150-155 ◽  
Author(s):  
M. Rita Young ◽  
Melvin E. Young ◽  
Yvonne Lozano ◽  
Michael Coogan ◽  
Jamila M. Bagash

2006 ◽  
Vol 95 (06) ◽  
pp. 1011-1018 ◽  
Author(s):  
Naoaki Harada ◽  
Hirotaka Isobe ◽  
Mitsuhiro Uchiba ◽  
Kenji Okajima

SummaryWe recently demonstrated that activation of the pulmonary sensory neurons plays a critical role in prevention of endotoxininduced shock by releasing calcitonin gene-related peptide (CGRP) in rats. CGRP increased the endothelial production of prostacyclin (PGI2) in the lungs, thereby preventing endotoxininduced shock response by inhibiting tumor necrosis factor-α (TNF-α) production. Since antithrombin (AT) enhances sensory neuron activation, we hypothesized that AT might reduce endotoxin-induced hypotension by enhancing the activation of pulmonary sensory neurons in rats. We examined this possibility using a rat model of endotoxin shock. AT-induced effects including reduction of hypotension (n=5) and inhibition of induction of iNOS (n=4 or 5) and TNF-α (n=5) in the lungs of endotoxin-treated animals were completely reversed by pretreatment with capsazepine (CPZ) (n=4 or 5), a vanilloid receptor antagonist, or CGRP(8–37), a CGRP receptor antagonist (n=4 or 5). AT enhanced endotoxin-induced increases in lung tissue levels of CGRP (n=4), but this effect of AT was not seen in animals pretreated with CPZ (n=4). CGRP produced therapeutic effects (n=5) similar to those induced by AT, and such therapeutic effects were completely abrogated by pretreatment with indomethacin (n=4). AT increased CGRP release from cultured dorsal root ganglion neurons only in the presence of anandamide (n=5),andAT-induced increase in CGRP release was not observed in the presence KT5720, an inhibitor of protein kinase A (n=5). AT markedly increased intracellular levels of cAMP in the presence of anandamide (n=5).These results strongly suggested that AT might reduce endotoxin-induced hypotension in rats by enhancing activation of sensory neurons via activation of protein kinase A.


Science ◽  
1993 ◽  
Vol 260 (5105) ◽  
pp. 222-226 ◽  
Author(s):  
B. Bacskai ◽  
B Hochner ◽  
M Mahaut-Smith ◽  
Adams ◽  
B. Kaang ◽  
...  

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