scholarly journals Activation of Platelet-activating Factor (PAF) Receptor Stimulates Nitric Oxide (NO) Release Via Protein Kinase C-α in HEC-1B Human Endometrial Epithelial Cell Line

2000 ◽  
Vol 6 (1) ◽  
pp. 37-49 ◽  
Author(s):  
Sharon Dearn ◽  
Mabhub Rahman ◽  
Aurélia Lewis ◽  
Zahra Ahmed ◽  
Margaret C. Eggo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Platelet Activating Factor ◽  
Epithelial Cell Line ◽  
Endometrial Epithelial Cell ◽  
Kinase C ◽  
No Release ◽  
Paf Receptor

Suppression of Protein Kinase C?? Triggers Apoptosis Through Down-Regulation of BCL-XL in a Rat Hepatic Epithelial Cell Line

Shock ◽  
2003 ◽  
Vol 19 (6) ◽  
pp. 582-587 ◽  
Author(s):  
Ya-Ching Hsieh ◽  
Hsiao-Ching Jao ◽  
Rei-Cheng Yang ◽  
Hseng-Kuang Hsu ◽  
Chin Hsu
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Cell Line ◽  
Epithelial Cell Line ◽  
Down Regulation ◽  
Kinase C

Multiple Signaling Pathways for Platelet-Activating Factor Receptor

Physiology ◽  
1992 ◽  
Vol 7 (2) ◽  
pp. 72-75
Author(s):  
SD Shukla
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
G Protein ◽  
Platelet Activating Factor ◽  
G Protein Coupled Receptors ◽  
Kinase C ◽  
Paf Receptor ◽  
Multiple Signaling ◽  
G Protein Coupled

Platelet-activating factor (PAF) receptor is coupled to multiple signaling pathways, including phospholipid turnover via phospholipases C, D, A2;Ca2+ mobilization;and activation of protein kinase C and tyrosine kinase. The cloned receptor shows homology to G protein-coupled receptors. These developments highlight receptor functions of this novel phospholipid agonist.

Muscarinic regulation of potassium transport in a human submandibular epithelial cell line

1990 ◽  
Vol 259 (2) ◽  
pp. C340-C348 ◽  
Author(s):  
J. A. Ship ◽  
L. L. Patton ◽  
R. B. Wellner
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Cell Line ◽  
Calcium Ionophore ◽  
Epithelial Cell Line ◽  
Ionophore A23187 ◽  
Muscarinic Agonist ◽  
Kinase C ◽  
86Rb Influx

Results of previous studies suggest that the transport of K+ by salivary ducts is under muscarinic control. The mechanisms by which this regulation occurs have not been well defined, however. In this paper, we describe mechanisms involved in the muscarinic regulation of K+ (86Rb) transport in HSG-PA, an epithelial cell line derived from human submandibular gland duct. Stimulation of HSG-PA cells by carbachol, a muscarinic agonist, increases both 86Rb influx and efflux, which results in a decrease in the equilibrium content of 86Rb within the cells. Increases in both fluxes are dose dependent with respect to carbachol concentration, and both responses can be blocked by atropine, a muscarinic antagonist. The carbachol-stimulated 86Rb fluxes appear to be calcium dependent since 1) the calcium ionophore A23187 increases 86Rb fluxes in these cells, 2) cells loaded with 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid (BAPTA; a calcium chelator) exhibit a reduced ability to respond to carbachol stimulation, and 3) removal of extracellular calcium concentration reduces the carbachol-stimulated effects. Treatment of HSG-PA cells with 10(-7) M phorbol myristate acetate (PMA) partially blocks the carbachol-stimulated changes in 86Rb fluxes, suggesting that protein kinase C plays a role in this response. PMA also partially blocks A23187-stimulated 86Rb influx, suggesting that activation of protein kinase C inhibits muscarinic-stimulated K+ influx by blocking either the Ca2+ signal (X. He, X. Wu, and B.J. Baum. Biochem. Biophys. Res. Commun. 152: 1062-1069, 1988), steps subsequent to this effect, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of protein kinase C in electrical-stimulation-induced neuronal nitric oxide release in mesenteric arteries from hypertensive rats

2000 ◽  
Vol 99 (4) ◽  
pp. 277-283 ◽  
Author(s):  
Jesús MARÍN ◽  
Mercedes FERRER ◽  
Gloria BALFAGÓN
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Protein Synthesis Inhibitor ◽  
Hypertensive Rats ◽  
Wky Rats ◽  
Kinase C ◽  
No Release

This study examines the influence of hypertension on neuronal nitric oxide (NO) release and its modulation by protein kinase C (PKC). For this purpose, mesenteric segments without endothelium were obtained from Wistar–Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs), and neurogenic NO release induced by electrical field stimulation (EFS) was examined in these segments. EFS induced frequency-dependent contractions. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the sensorial neurotoxin capsaicin increased EFS-induced contractions in SHR segments, but did not affect these contractions in segments from WKY rats. In segments from SHRs, the increase in EFS-induced response by capsaicin was further increased by the combination of capsaicin and L-NAME. EFS-induced contractions in SHR arteries were unaltered by the protein synthesis inhibitor cycloheximide or by 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), an inhibitor of inducible NO synthase, and increased by the guanylate cyclase inhibitor Methylene Blue. In these arteries, capsaicin plus the PKC inhibitor calphostin C increased the contractions elicited by EFS; the addition of L-NAME did not affect this increase. Phorbol 12,13-dibutyrate (PDBu) did not modify the response to EFS in these arteries pretreated with capsaicin, although a combination of PDBu and L-NAME was effective. These results indicate that, in mesenteric arteries, EFS induces the release of NO from perivascular nitrergic nerves and of neuropeptides from sensory nerves, but only in hypertensive rats. The NO released is synthesized by constitutive neuronal NO synthase in a manner that is positively modulated by PKC, an enzyme that seems to be activated in hypertension.

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