Angiotensin II stimulates apoptosis via TGF-β1 signaling in ventricular cardiomyocytes of rat

2006 ◽  
Vol 84 (11) ◽  
pp. 975-983 ◽  
Author(s):  
D. Schröder ◽  
J. Heger ◽  
H. M. Piper ◽  
G. Euler
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Cardiomyocytes ◽  
Tgf Β1

scholarly journals Fus knockdown inhibits the profibrogenic effect of cardiac fibroblasts induced by angiotensin II through targeting Pax3 thereby regulating TGF-β1/Smad pathway

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 1415-1425
Author(s):  
Guoqiang Wang ◽  
Hong Wu ◽  
Peng Liang ◽  
Xiaojiao He ◽  
Dong Liu
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblasts ◽  
Smad Pathway ◽  
Tgf Β1

Contributions of angiotensin II and tumor necrosis factor-α to the development of renal fibrosis

2001 ◽  
Vol 280 (5) ◽  
pp. F777-F785 ◽  
Author(s):  
Guangjie Guo ◽  
Jeremiah Morrissey ◽  
Ruth McCracken ◽  
Timothy Tolley ◽  
Helen Liapis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Tumor Necrosis Factor ◽  
Renal Fibrosis ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Wild Type ◽  
Tnf Α ◽  
Factor Α ◽  
Tgf Β1 ◽  
Necrosis Factor

Angiotensin II upregulates tumor necrosis factor-α (TNF-α) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-α receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT1a or the TNF-α receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vvint) in the C57BI/6 wild-type mouse was decreased in the AT1a KO from 32.8 ± 4.0 to 21.0 ± 3.7% ( P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 ± 2.1% ( P < 0.005). The Vvint of the TNFR1/TNFR2 KO was further decreased to 15.2 ± 3.7% ( P < 0.01) by enalapril compared with no treatment. The induction of TNF-α mRNA and transforming growth factor-β1 (TGF-β1) mRNA in the kidney with UUO was significantly blunted in the AT1a or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-α and TGF-β1 mRNA and their proteins to near normal levels. Also, α-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT1a or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-α systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy.

Pioglitazone inhibits angiotensin II-induced atrial fibroblasts proliferation via NF-κB/TGF-β1/TRIF/TRAF6 pathway

2015 ◽  
Vol 330 (1) ◽  
pp. 43-55 ◽  
Author(s):  
Xiao-qing Chen ◽  
Xu Liu ◽  
Quan-xing Wang ◽  
Ming-jian Zhang ◽  
Meng Guo ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Tgf Β1

Angiotensin II induces TGF-β1 production in rat heart endothelial cells

1994 ◽  
Vol 1223 (1) ◽  
pp. 141-147 ◽  
Author(s):  
Chu Chang Chua ◽  
Clement A. Diglio ◽  
Bun Brian Siu ◽  
Balvin H.L. Chua
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Rat Heart ◽  
Tgf Β1

Upregulation of α8β1-integrin in cardiac fibroblast by angiotensin II and transforming growth factor-β1

2001 ◽  
Vol 281 (5) ◽  
pp. C1457-C1467 ◽  
Author(s):  
Gaétan Thibault ◽  
Marie-Josée Lacombe ◽  
Lynn M. Schnapp ◽  
Alexandre Lacasse ◽  
Fatiha Bouzeghrane ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Matrix Protein ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Transforming Growth Factor Β1 ◽  
Cardiac Fibroblast ◽  
Extracellular Matrix Protein ◽  
Ang Ii ◽  
Tgf Β1

Using a novel pharmacological tool with125I-echistatin to detect integrins on the cell, we have observed that cardiac fibroblasts harbor five different RGD-binding integrins: α8β1, α3β1, α5β1, αvβ1, and αvβ3. Stimulation of cardiac fibroblasts by angiotensin II (ANG II) or transforming growth factor-β1 (TGF-β1) resulted in an increase of protein and heightening by 50% of the receptor density of α8β1-integrin. The effect of ANG II was blocked by an AT1, but not an AT2, receptor antagonist, or by an anti-TGF-β1 antibody. ANG II and TGF-β1 increased fibronectin secretion, smooth muscle α-actin synthesis, and formation of actin stress fibers and enhanced attachment of fibroblasts to a fibronectin matrix. The α8- and β1-subunits were colocalized by immunocytochemistry with vinculin or β3-integrin at focal adhesion sites. These results indicate that α8β1-integrin is an abundant integrin on rat cardiac fibroblasts. Its positive modulation by ANG II and TGF-β1 in a myofibroblast-like phenotype suggests the involvement of α8β1-integrin in extracellular matrix protein deposition and cardiac fibroblast adhesion.

scholarly journals Angiotensin II increases periostin expression via Ras/p38 MAPK/CREB and ERK1/2/TGF-β1 pathways in cardiac fibroblasts

2011 ◽  
Vol 91 (1) ◽  
pp. 80-89 ◽  
Author(s):  
Li Li ◽  
Dong Fan ◽  
Cheng Wang ◽  
Jin-Yu Wang ◽  
Xiao-Bing Cui ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
P38 Mapk ◽  
Cardiac Fibroblasts ◽  
Tgf Β1

scholarly journals P517Autocrine angiotensin II-signaling in FGF23-induced Ca2+-mediated hypertrophy in ventricular cardiomyocytes

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S126-S126
Author(s):  
K N Mhatre ◽  
P Wakula ◽  
E Bisping ◽  
B Pieske ◽  
F Heinzel
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Cardiomyocytes ◽  
Angiotensin Ii Signaling

scholarly journals Endogenous CCN5 Participates in Angiotensin II/TGF-β1 Networking of Cardiac Fibrosis in High Angiotensin II-Induced Hypertensive Heart Failure

2020 ◽  
Vol 11 ◽  
Author(s):  
Anan Huang ◽  
Huihui Li ◽  
Chao Zeng ◽  
Wanli Chen ◽  
Liping Wei ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Fibrosis ◽  
Tgf Β1

scholarly journals Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (6) ◽  
pp. 1065-1071 ◽  
Author(s):  
Susana Ravassa ◽  
María Antonia Fortuño ◽  
Arantxa González ◽  
Begoña López ◽  
Guillermo Zalba ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ventricular Cardiomyocytes ◽  
Induced Apoptosis ◽  
Increased Susceptibility

Iron chelation and a free radical scavenger suppress angiotensin II-induced upregulation of TGF-β1 in the heart

2005 ◽  
Vol 288 (4) ◽  
pp. H1836-H1843 ◽  
Author(s):  
Kan Saito ◽  
Nobukazu Ishizaka ◽  
Toru Aizawa ◽  
Masataka Sata ◽  
Naoyuki Iso-o ◽  
...  
Keyword(s):  
Free Radical ◽  
Angiotensin Ii ◽  
Cardiac Fibrosis ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Heme Oxygenase 1 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Tgf Β1

Long-term administration of angiotensin II causes myocardial loss and cardiac fibrosis. We previously found iron deposition in the heart of the angiotensin II-infused rat, which may promote angiotensin II-induced cardiac damage. In the present study, we have investigated whether an iron chelator (deferoxamine) and a free radical scavenger (T-0970) affect the angiotensin II-induced upregulation of transforming growth factor-β1 (TGF-β1). Angiotensin II infusion for 7 days caused a robust increase in TGF-β1 mRNA expression in vascular smooth muscle cells, myofibroblast-like cells, and migrated monocytes/macrophages. T-0970 and deferoxamine suppressed the upregulation of TGF-β1 mRNA and reduced the extent of cardiac fibrosis in the heart of rats treated with angiotensin II. These agents blocked the angiotensin II-induced upregulation of heme oxygenase-1, a potent oxidative and cellular stress-responsive gene, but they did not significantly affect systolic blood pressure or plasma levels of aldosterone. In addition, T-0970 and deferoxamine suppressed the angiotensin II-induced upregulation of monocyte chemoattractant protein-1 in the heart. These results collectively suggest that iron and the iron-mediated generation of reactive oxygen species may contribute to angiotensin II-induced upregulation of profibrotic and proinflammatory genes, such as TGF-β1 and monocyte chemoattractant protein-1.

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