◀ Back to ANGPT2

ANGPT2 — TGFB1

Text-mined interactions from Literome

Wenzel et al., Kidney Int 2002 (Glomerulonephritis, Membranoproliferative) : Ang II induced the glomerular expression of the cell cycle inhibitor p27KIP1 and of transforming growth factor-beta ( TGF-beta ) and inhibited expression of monocyte chemotactic protein 1 (MCP-1)
Ding et al., American journal of physiology. Renal physiology 2002 : Moreover, ANG II stimulated transforming growth factor (TGF)-beta1 production as measured by ELISA
Weigert et al., Diabetologia 2002 (Hyperglycemia) : Because previous in vitro studies demonstrated the angiotensin II (ang II) mediated up-regulation of the prosclerotic transforming growth factor beta 1 (TGF) we studied the molecular mechanism of ang II-induced TGF-beta 1 gene activation ... The findings indicate that ang II and hyperglycaemia stimulate the TGF-beta 1 gene activation through the same PKC- and p38 MAPK dependent pathways by the same regulatory elements of the TGF-beta 1 promoter
Kawaguchi et al., Arthritis Rheum 2004 (Fibrosis...) : Exogenous Ang II augmented the production of type I procollagen and transforming growth factor beta1 by cultured fibroblasts via activation of AT(1)
Rosenkranz et al., Cardiovasc Res 2004 (Cardiomyopathy, Dilated...) : Ang II upregulates TGF-beta1 expression via activation of the angiotensin type 1 (AT1) receptor in cardiac myocytes and fibroblasts, and induction of this cytokine is absolutely required for Ang II-induced cardiac hypertrophy in vivo
Gibbons et al., J Clin Invest 1992 (Hyperplasia...) : We conclude that : ( a ) Ang II induces increased TGF beta 1 gene expression via a PKC dependent pathway involving de novo protein synthesis ; ( b ) Ang II promotes the conversion of latent TGF beta 1 to its biologically active form ; ( c ) Ang II modulates VSMC growth by activating both proliferative and antiproliferative pathways ; and ( d ) Autocrine active TGF beta 1 appears to be an important determinant of VSMC growth by hypertrophy or hyperplasia
Han et al., Nephrol Dial Transplant 2006 (Diabetic Nephropathies) : In cultured cells, both high glucose and Ang-II induced significant increases in TGF-beta1 , TIMP-2, and in collagen synthesis, and significant decreases in MMP-2 gene expression and activity, and thus disrupted the balance between MMP-2 and TIMP-2
Martin et al., Am J Physiol Lung Cell Mol Physiol 2007 (MAP Kinase Signaling System) : Interactions between the renin-angiotensin system (RAS) and TGF-beta1 have been well documented, with most studies describing the effect of ANG II on TGF-beta1 expression
de Cavanagh et al., Am J Physiol Heart Circ Physiol 2009 (Cardiovascular Diseases) : ANG II-initiated integrin signaling results in the release of transforming growth factor-beta(1) ( TGF-beta(1) ), a cytokine that modifies ECM composition and structure, induces reorganization of the cytoskeleton, and modifies mitochondrial function
Kim et al., J Cell Physiol 2010 (Calcium Signaling...) : High glucose or ANG II also synergistically increased transforming growth factor-beta1 ( TGF-beta(1) ) expression, while pretreatment with losartan abolished the high glucose induced increase in TGF-beta(1) production
Zhang et al., Hypertension 2010 (Fibrosis...) : Enhanced upregulation of the Ang II type I receptor and activation of the transforming growth factor-beta/Smad and nuclear factor-kappaB signaling pathways may be the mechanisms by which CRP promotes cardiac fibrosis and inflammation under high Ang II conditions
Singh et al., Journal of signal transduction 2011 : Also inhibition of Ang II formation in cell media ( extracellular ) and lysates ( intracellular ) blocks high-glucose effects on TGF-b1 and matrix more effectively compared to inhibition of extracellular Ang II alone ... These findings suggest that intracellular Ang II increases TGF-b1 and matrix in human mesangial cells and also activates Stat3 transcription factor without involvement of the extracellular Ang II signaling pathway
Morales et al., Int J Biochem Cell Biol 2012 (Fibrosis) : In this paper, we show that in myoblasts, Ang-II induced the increase of transforming growth factor beta 1 ( TGF-ß1 ) and connective tissue growth factor (CTGF) expression through its AT-1 receptor
Wolf et al., Nephrol Dial Transplant 1996 : In addition, Ang II also induces the expression of TGF-beta1 in these cells
Anderson et al., Kidney Int 1996 : Ang II alone ( 1 microM ) added to quiescent, murine mesangial cells in serum-free, insulin-free media slightly but not significantly increased TGF-beta 1 , fibronectin, collagen I, collagen IV and laminin message levels ... Ang II plus insulin further significantly increased collagen I ( 9-fold ), collagen IV ( 9-fold ), fibronectin 1 ( 5-fold ) and TGF-beta 1 ( 3-fold ) message expression
Shihab et al., Kidney Int 1997 (Kidney Diseases) : Similarly, Ang II blockade resulted in decreased expression of TGF-beta1 and PAI-1 by Northern and ELISA