Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Tumor necrosis factor-alpha regulates inducible nitric oxide synthase gene expression in the portal hypertensive gastric mucosa of the rat.

Authors: Kaviani, A  Ohta, M  Itani, R  Sander, F  Tarnawski, A S  Sarfeh, I J 
Citation: Kaviani A, etal., J Gastrointest Surg. 1997 Jul-Aug;1(4):371-6.
Pubmed: (View Article at PubMed) PMID:9834372

Increased expression of both nitric oxide synthase (NOS) and tumor necrosis factor-alpha (TNF-alpha) have been implicated in the hyperdynamic circulation of portal hypertension. Since overexpression of these proteins would affect gastric mucosal defenses, which are impaired in portal hypertension, we examined the expression and interrelationships of TNF-alpha and NOS in the gastric mucosa of portal hypertensive rats. Following staged portal vein ligation, gastric strips from portal hypertensive rats were incubated in organ culture medium with or without TNF-alpha antibody. The expression of TNF-alpha and NOS mRNAs was assessed by reverse transcription-polymerase chain reaction (RT-PCR) at baseline and after 1, 2, and 6 hours of incubation. RT-PCR demonstrated a threefold increase in inducible NOS mRNA and a 50% increase in TNF-alpha mRNA expression at baseline in portal hypertensive animals as compared to sham-operated animals. In tissue incubated with TNF-alpha neutralizing antibody, inducible NOS mRNA expression was significantly decreased by 40%, 70%, and 80% after 1, 2, and 6 hours, respectively. Since increased TNF-alpha and NOS production could potentially impair gastric mucosal defenses, our findings suggest a major role for these proteins in the development of portal hypertensive gastropathy.


Disease Annotations
Gene Ontology Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 14688051
Created: 2019-06-06
Species: All species
Last Modified: 2019-06-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.