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ANG — TGFB1

Text-mined interactions from Literome

Nakamura et al., Kidney Int 1999 (Disease Models, Animal...) : Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta ( TGF-beta ) and extracellular matrix components
Hamaguchi et al., Hypertension 1999 (Hypertension) : We have previously demonstrated that angiotensin II (Ang II) contributes to the increase in aortic transforming growth factor-beta(1) ( TGF-beta(1) ) mRNA levels in hypertensive rats
Yoo et al., Am J Physiol Regul Integr Comp Physiol 2000 (Ureteral Obstruction) : ANG stimulated renal TGF-beta1 expression via AT(1) receptors, a response similar to that in the adult
Kupfahl et al., Cardiovasc Res 2000 : In the human heart, Ang II does not directly increase collagen or fibronectin mRNA, but it does increase TGFbeta-1 and osteopontin mRNA expression
Schultz et al., J Clin Invest 2002 (Cardiomegaly) : Angiotensin II (Ang II) , a potent hypertrophic stimulus, causes significant increases in TGFb1 gene expression
Ding et al., American journal of physiology. Renal physiology 2002 : Moreover, ANG II stimulated transforming growth factor (TGF)-beta1 production as measured by ELISA
Di Paolo et al., Transplantation 2002 : Ang II ( 100 pM ) strongly inhibited TGF-beta1 synthesis by PBMC, and such effect was completely abolished by the addition of 200 ng/mL CsA, as well as by 1 micrpM losartan ... Thus, captopril enhances TGF-beta1 gene and protein expression by PBMC by way of a mechanism independent, at least in part, from ACE inhibition, while CsA abrogates the inhibition of TGF-beta1 expression induced by Ang II
Sharma et al., American journal of physiology. Renal physiology 2003 (Diabetes Mellitus, Experimental...) : We postulated that diabetes induced transforming growth factor ( TGF ) -beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels
Okada et al., Am J Nephrol 2004 (Fibrosis...) : Ang II alone could not induce gene expression of a pro-inflammatory chemokine JE or a pro-fibrotic cytokine transforming growth factor-beta1 in those cells
Fukami et al., Kidney Int 2004 : In this study, we investigated whether AGEs could activate autocrine angiotensin II (Ang II) signaling and subsequently induce transforming growth factor-beta ( TGF-beta ) -Smad signaling in cultured rat mesangial cells
Chen et al., Toxicology 2005 (Disease Models, Animal...) : Angiotensin II (Ang II) is an inducer of TGF-beta1 in cells of the heart and kidneys, and the regulation of TGF-beta1 by Ang II has not yet been confirmed in lung tissue
Gibbons et al., J Clin Invest 1992 (Hyperplasia...) : Because transforming growth factor-beta 1 ( TGF beta 1 ) has similar bifunctional effects on VSMC growth, we hypothesized that autocrine production of TGF beta 1 may mediate the growth modulatory effects of Ang II
Brezniceanu et al., Kidney Int 2006 : Stable transfer of p53 cDNA ( S ) enhanced and p53 cDNA ( AS ) abolished the stimulatory effect of TGF-beta1 on ANG mRNA expression in IRPTCs
Lee et al., Nephrol Dial Transplant 2007 (Diabetes Mellitus, Experimental...) : COMP-Ang1 also reduced renal tissue levels of transforming growth factor-beta1 ( TGF-beta1 ), alpha-smooth muscle actin, fibronectin, as well as Smad 2/3 expression, but increased Smad 7 expression
El Chaar et al., American journal of physiology. Renal physiology 2007 (Fibrosis...) : Both transforming growth factor-beta ( TGF-beta ) and ANG II have been implicated, and ANG II may mediate its effects through TGF-beta
Yurovsky et al., Am J Hypertens 2007 (Fibrosis) : Angiotensin II ( Ang ) has been shown to induce expression of transforming growth factor-beta1 ( TGF-beta1 ) in cardiovascular cells in vitro, but the regulation of TGF-beta1 by Ang has not been shown in cerebral vessels in vivo
Zimpelmann et al., American journal of physiology. Renal physiology 2009 (MAP Kinase Signaling System) : Ang- ( 1-7 ) significantly enhanced DNA synthesis and increased production of transforming growth factor-beta1 ( TGF-beta1 ), fibronectin, and collagen IV ... Stimulation of p38 MAPK phosphorylation by Ang- ( 1-7 ) leads to release of arachidonic acid and production of TGF-beta1 and extracellular matrix proteins
Gava et al., Nephrol Dial Transplant 2009 (Diabetic Nephropathies) : Ang- ( 1-7 ) inhibited high glucose stimulated protein synthesis, and blocked the stimulatory effect of glucose on TGF-beta1
Zeng et al., Biochem Biophys Res Commun 2009 : Interestingly, the levels of circulating transforming growth factor-beta1 ( TGF-beta1 ) after myocardial infarction were suppressed by ANG- ( 1-7 ), which suggests a possible downstream target for the anti remodeling action of ANG- ( 1-7 ) ... Furthermore, the expression of TGF-beta1 and phosphor-Smad2 ( p-Smad2 ) were significantly suppressed by ANG- ( 1-7 ) ( vs. Control group : 1.21+/-0.07 vs. 1.54+/-0.08, P < 0.001 and 0.31+/-0.01 vs. 0.43+/-0.02, P < 0.001, respectively ), but no effect on p38 phosphorylation was observed
Kim et al., Am J Physiol 1995 (Cardiomegaly) : In addition, studies using antibodies and bioassay for transforming growth factor-beta 1 ( TGF-beta 1 ) suggested that TGF-beta 1 does not mediate the trophic effects of ANG II on NM
Lee et al., J Mol Cell Cardiol 1995 (Cardiomegaly...) : In the present study, we postulated that Ang II action in adult cardiac fibroblasts may stimulate the autocrine production and release of transforming growth factor-beta 1 ( TGF-beta 1 ), a known regulator of cardiac fibroblast and myocyte function
Campbell et al., J Mol Cell Cardiol 1997 (Myocardial Infarction) : Ang II stimulated further TGF-beta1 secretion in VIC and CFb, but not MyoFb ... Ang II stimulates TGF-beta1 gene expression and/or protein production in cardiac fibroblast-like cells which may act as an autocrine/paracrine stimulus to collagen formation
Shihab et al., Kidney Int 1997 (Kidney Diseases) : These results suggest that CsA induced fibrosis in this model is independent of renal hemodynamics and is mediated, at least partly, through Ang II induction of TGF-beta1 expression
Harada et al., Circulation 1997 (Cardiomegaly...) : Angiotensin II (Ang II) ( 10 ( -10 ) to 10 ( -6 ) mol/L ) and transforming growth factor-beta1 ( TGF-beta1 ) ( 10 ( -13 ) to 10 ( -9 ) mol/L ), both of which are known to be cardiac hypertrophic factors, did not induce hypertrophy in MC culture, but both Ang II and TGF-beta1 increased the size of MCs and augmented ANP and BNP productions in the MC-NMC coculture