Document Detail


PGE2 enhances cytokine-elicited nitric oxide production in mouse cortical collecting duct cells.
MedLine Citation:
PMID:  15797843     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It has been documented that arginine vasopressin (AVP) and prostaglandin E(2) (PGE(2)) regulate water reabsorption in renal tubular cells. The present study was attempted to delineate the downstream signaling of AVP and PGE(2) in a cortical collecting duct cell line (M-1 cell). Using RT-PCR, we detected mRNA for V2 and VACM-1 but not for V1a and AII/AVP receptors of AVP. Furthermore, neither AVP nor V2 receptor agonist and antagonist alter cellular cAMP. These together with unchanged cellular Ca(2+) by AVP suggested that AVP pathway was not operating in M-1 cells. All four classical PGE(2) receptors with EP3 and EP4 as the most prominent were detected in M-1 cells. PGE(2), 11-deoxy-PGE(1) (EP2 and EP4 agonist), and 17-phenyl-trinor-PGE(2) (EP1 agonist) increased cellular concentration of cAMP. There was no effect of PGE(2) or EP1 agonist on cellular Ca(2+). These findings provide evidence of the involvement of PGE(2) cascade in M-1 cells. M-1 cells were capable of synthesizing nitric oxide (NO). Although individual cytokines did not affect NO production, a mixture of tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma elevated NO concentration to 4.5-fold of the control. Addition of PGE(2) and db-cAMP to the cytokine mixture further increased NO production to 7.0- and 9.8-fold, respectively, of that seen in non-treated cells. PGE(2) or db-cAMP alone, however, had no effect on NO production. The results of the study led us to speculate that enhanced production of cAMP via PGE(2) signaling pathway in M-1 cells could either stimulate or attenuate water reabsorption in renal tubule. While an increase in cAMP alone may enhance water reabsorption, a concomitant increase in cAMP and cytokines may inhibit water reabsorption in renal tubule.
Authors:
Chien-Ning Huang; Kai-Li Liu; Chun-Hsu Cheng; Yu-Sheng Lin; Min-Jon Lin; Ting-Hui Lin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society     Volume:  12     ISSN:  1089-8603     ISO Abbreviation:  Nitric Oxide     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-03-30     Completed Date:  2005-08-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9709307     Medline TA:  Nitric Oxide     Country:  United States    
Other Details:
Languages:  eng     Pagination:  150-8     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Internal Medicine, Chung Shan Medical University, Number 110, Section 1, Chien-Kuo North Road, Taichung 40203, Taiwan, ROC.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arginine Vasopressin / physiology
Base Sequence
Cell Line
Cyclic AMP / biosynthesis
Cytokines / pharmacology*
Dinoprostone / physiology*
Ionomycin / pharmacology
Kidney Tubules, Collecting / chemistry,  metabolism*
Mice
Molecular Sequence Data
Nitric Oxide / biosynthesis*,  physiology
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type II
Receptors, Prostaglandin E / analysis,  genetics
Receptors, Vasopressin / analysis,  genetics
Renal Agents / pharmacology
Signal Transduction
Chemical
Reg. No./Substance:
0/Cytokines; 0/Receptors, Prostaglandin E; 0/Receptors, Vasopressin; 0/Renal Agents; 0/vasotocin receptor; 10102-43-9/Nitric Oxide; 113-79-1/Arginine Vasopressin; 363-24-6/Dinoprostone; 56092-81-0/Ionomycin; 60-92-4/Cyclic AMP; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse

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