IndraLab
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"In the present study, we demonstrate that the inhibition of PI3K in VSMCs by expression of a dominant negative p85alpha mutant lacking the p110 binding domain (Deltap85), or by treatment of cells with LY294002, inhibited Ang II stimulated PAI-1 (plasminogen activator inhibitor-1) mRNA expression."
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"Because the expression of TF and PAI-1 mRNA induced by Ang II was attenuated by the increase of intracellular concentrations of cAMP by forskolin and 8-bromo-cAMP and because AM increased the intracellular level of cAMP in rat aortic endothelial cells, it was indicated that the inhibitory effect of AM on the expressions of TF and PAI-1 was mainly mediated by the cAMP dependent signal transduction."
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"The membrane-permeant cGMP analogue 8-Br-cGMP reduced Ang II stimulated PAI-1 expression by 60%, and an inhibitor of soluble guanylyl cyclase (1H-[1,2,4] oxadiazolo [4, 3-a] quinoxalin-1-one) significantly impaired the inhibitory effects of S-nitroso-N-acetylpenicillamine on Ang II stimulated PAI-1 expression."
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"Although PAI-1 gene expression was also stimulated by Ang II in neuronal cultures of SH rat brain, two differences between WKY and SH rat brain neurons were observed : 1) the level of Ang II stimulation in SH rat neurons was 50% of that in WKY rat neurons; and 2) Ang II stimulation of c-fos was 2.4-fold higher in SH neurons than in WKY neurons, but c-fos antisense oligonucleotide did not attenuate the stimulatory action of Ang II on PAI-1 mRNA in SH neurons."
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"The apelins-12 and -13 inhibit the vasoconstrictive effect of Ang-II and confers beneficial cardiovascular effects through ACE2/Ang(1-7)-and/or Larginine/endothelial nitric oxide synthase (eNOS)/nitric oxide (NO)-dependent and vascular remodeling through blocking Ang II-induced PAI-1 gene expression and increasing NO production [16]."
| PMC
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"In the present study, we demonstrate that brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) interact with angiotensin II (Ang II) in regulative blood coagulation and fibrinolysis by suppressing the expressions of both tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) induced by Ang II."
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"For example, activation of angiotensin-1 type-4 receptors, bradykinin type-2 and endothelin-1 A receptors have all been linked to the increased expression and elevated plasma levels of PAI-1 elicited by AngII, and the same receptors have been implicated in AngII mediated arteriolar thrombosis [XREF_BIBR, XREF_BIBR], suggesting a cause-effect relationship between the elevated PAI-1 level and accelerated arteriolar thrombosis."
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"Spironolactone (10 -6 M) prevented Ang II stimulated PAI-1 mRNA expression and attenuated the effect of Ang II + aldosterone on PAI-1 expression such that the PAI-1 mRNA expression was similar to that after treatment with aldosterone alone but still increased compared with control."
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"This study aimed to identify the intracellular signaling pathway in angiotensin II (Ang II)-induced upregulation of plasminogen activator inhibitor type 1 (PAI-1) mRNA expression in cultured rat glomerular mesangial cells, and to examine the interaction between Ang II and TGF-beta signaling."