Linked Life Data

16820795

Source:http://linkedlifedata.com/resource/pubmed/id/16820795

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-8-24
pubmed:abstractText
Prostanoids exert physiological effects on ureteral contractility that may lead to pressure changes and pain during obstruction. In the present study, we examined whether (1) obstruction changes the expression of the two cyclooxygenase (COX) isoforms, COX-1 and COX-2 in human and rat ureters and (2) administration of a selective COX-2 inhibitor influences the pelvic pressure change after experimental ureteral obstruction. Rats were subjected to bilateral ureter obstruction. Ureters were removed and dissected into a proximal dilated and distal non-dilated segment. RNA and protein were extracted and analyzed for cyclooxygenase expression by quantitative polymerase chain reaction and Western blotting. Human ureter samples were obtained from patients undergoing radical nephrectomy. Rat and human ureteral samples were processed for immunohistochemistry. COX-1, but not COX-2 mRNA, was readily detected in the normal rat ureter. COX-2 mRNA and protein expression was increased in the proximal dilated ureter compared to distal non-dilated ureter. This increased COX-2 expression was associated with increased urinary prostaglandin E2 (PGE2) excretion after release of obstruction. Immunohistochemistry showed increased COX-2 labeling in surface epithelium and smooth muscle layers in both rat and human obstructed ureters compared to control ureters. Furthermore, contractile PGE2-EP1 and thromboxane TP receptors were expressed in ureteral smooth muscle. Systemic treatment with the COX-2 selective inhibitor parecoxib (5 mg/kg/day) attenuated the pelvic pressure increase during obstruction. In summary, COX-2 expression is significantly increased in the ureteral wall in response to obstruction in the rat and human ureter and COX-2 activity contributes to increased pelvic pressure after obstruction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
872-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16820795-Animals, pubmed-meshheading:16820795-Cyclooxygenase 1, pubmed-meshheading:16820795-Cyclooxygenase 2, pubmed-meshheading:16820795-Cyclooxygenase 2 Inhibitors, pubmed-meshheading:16820795-Dinoprostone, pubmed-meshheading:16820795-Gene Expression Regulation, pubmed-meshheading:16820795-Gene Expression Regulation, Enzymologic, pubmed-meshheading:16820795-Humans, pubmed-meshheading:16820795-Isoxazoles, pubmed-meshheading:16820795-Male, pubmed-meshheading:16820795-Membrane Proteins, pubmed-meshheading:16820795-Pelvis, pubmed-meshheading:16820795-Pressure, pubmed-meshheading:16820795-RNA, Messenger, pubmed-meshheading:16820795-Rats, pubmed-meshheading:16820795-Rats, Wistar, pubmed-meshheading:16820795-Receptors, Prostaglandin, pubmed-meshheading:16820795-Ureter, pubmed-meshheading:16820795-Ureteral Obstruction
pubmed:year
2006
pubmed:articleTitle
Cyclooxygenase type 2 is increased in obstructed rat and human ureter and contributes to pelvic pressure increase after obstruction.
pubmed:affiliation
The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't