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NOS2 — RHOA
Text-mined interactions from Literome
Kreiselmeier et al., Am J Physiol Lung Cell Mol Physiol 2003
(Adenocarcinoma, Bronchiolo-Alveolar...) :
Previous evidence also suggests that
NOS2 expression can be negatively
regulated by increased activation of the GTPase
RhoA , leading to the hypothesis that CF-related increases in PIAS1 expression and altered STAT1 signaling may be mediated by Rho GTPase function
Rattan et al., Free Radic Biol Med 2003
:
Rho A negatively
regulates cytokine mediated inducible
nitric oxide synthase expression in brain derived transformed cell lines : negative regulation of IKKalpha ... Taken together, these studies show that downregulation of
RhoA by lovastatin
resulted in increased
iNOS expression via the activation of NF-kappaB-CBP/p300 pathway in transformed brain cells
Bivalacqua et al., Proc Natl Acad Sci U S A 2004
(Body Weight...) :
RhoA/Rho-kinase suppresses endothelial
nitric oxide synthase in the penis : a mechanism for diabetes associated erectile dysfunction
Liao et al., J Investig Med 2004
(Cardiomegaly...) :
Furthermore, inhibition of
RhoA by statins
leads to the activation of protein kinase B/Akt and up-regulation of endothelial
nitric oxide synthase in the endothelium and the heart
Mital et al., Semin Vasc Med 2004
(Cardiomegaly) :
Furthermore, inhibition of
RhoA by statins
leads to the activation of protein kinase B/Akt and upregulation of Type 3
nitric oxide synthase in the endothelium and the heart
Trebicka et al., Hepatology 2007
(Liver Cirrhosis) :
Atorvastatin lowers portal pressure in cirrhotic rats by inhibition of
RhoA/Rho-kinase and
activation of endothelial
nitric oxide synthase
Soliman et al., Cardiovasc Res 2008
(Diabetes Mellitus, Experimental...) :
Role of inducible
nitric oxide synthase in induction of
RhoA expression in hearts from diabetic rats ... Therefore, in this study, we investigated the hypothesis that induction of
iNOS positively
regulates RhoA expression in diabetic rat hearts ... To determine whether NO and
iNOS could
increase RhoA expression in the heart, cardiomyocytes from non-diabetic rats were cultured in the presence of the NO donor sodium nitroprusside ( SNP ) or lipopolysaccharide (LPS) in the absence and presence of the selective iNOS inhibitor, N ( 6 ) - ( 1-iminoethyl ) -l-lysine dihydrochloride ( L-NIL ) ... In a second study, 1 week after induction of diabetes with STZ, rats were treated with L-NIL ( 3 mg/kg/day ) for 8 more weeks to determine the
effect of
iNOS inhibition in vivo on
RhoA expression and cardiac contractile function ... These data suggest that
iNOS is
involved in the increased expression of
RhoA in diabetic hearts and that one of the mechanisms by which iNOS inhibition improves cardiac function is by preventing the upregulation of RhoA and its availability for activation
Soliman et al., Am J Physiol Heart Circ Physiol 2012
(Diabetes Mellitus, Experimental...) :
Inhibition of
RhoA and ROCK markedly
attenuated the diabetes induced increases in PKCß ( 2 ) activity and
iNOS and RhoA expression in diabetic cardiomyocytes, while having no effect in control cells
Tong et al., Inflammation 2013
:
Taken together, our findings suggest that
iNOS mediated activation of
RhoA appears to be one of the important mechanisms contributing to the deleterious effects of alcohol on intestinal barrier function