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

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 GW26-e0186 Triptolide inhibits angiotensin II induced cardiac fibroblasts proliferation by down-regulating TGF-β1/Smad3 pathway

2015 ◽  
Vol 66 (16) ◽  
pp. C95
Author(s):  
Jian Chen ◽  
Mao Liu ◽  
James Yeh ◽  
Wenyi Tang ◽  
Guangyi Tan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblasts ◽  
Tgf Β1

scholarly journals Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Gabriela Placoná Diniz ◽  
Marcela Sorelli Carneiro-Ramos ◽  
Maria Luiza Morais Barreto-Chaves
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Angiotensin Ii Receptors ◽  
Cardiomyocyte Hypertrophy ◽  
Tgf Β1

TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

scholarly journals Epicardial adipose tissie-derived leptin induce MMPs/TIMPs imbalance and promotes myocardial remodeling in high fat diet-induced obese rats

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
G Tian ◽  
L Liu ◽  
C D Luo ◽  
M Li ◽  
L F Cao ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
High Fat Diet ◽  
Type I Collagen ◽  
Nuclear Translocation ◽  
Cardiac Fibroblasts ◽  
Type I ◽  
Myocardial Remodeling ◽  
High Fat ◽  
Obese Rats ◽  
Tgf Β1

Abstract Background and aims Epicardial adipose tissue (EAT)-derived leptin contributes to myocardial remodeling in metabolic syndrome. However, the precise mechanisms remain to be determined. The present study was designed to elucidate the adverse effects of EAT-derived leptin on obesity-related myocardial remodeling. Methods and results Eight-week-old male Wistar rats were divided into two groups that received either a normal diet (control, n=10) or a high-fat diet (obese, n=10) for 12 weeks. Obese rats exhibited abnormal myocardial structure, diastolic dysfunction and abundant collagen deposition. Local leptin expression in obese rats EAT upregulated along with adipocyte hypertrophy, accompanied by renin-angiotensin-aldosterone system (RAAS) activation and increased oxidative stress level. Leptin receptor (ObR) and angiotensin II type 1 receptor (AT1R) expression in obese EAT were significantly higher than that in control. In vitro, mature adipocytes treated with angiotensin II (Ang II) exhibited pronounced leptin synthesis and secretion by promoting AP-1 nuclear translocation via the AT1R-ROS-ERK1/2 pathway. Moreover, cardiac fibroblasts were incubated with obese rat EAT-conditioned medium (EAT-CM), plus various inhibitors. EAT-derived leptin promoted proliferation of cardiac fibroblasts associated with increased ERK1/2 phosphorylation and induced MMPs/TIMPs imbalance, stimulating upregulation of type I collagen via the JAK2/STAT3-TGF-β1/Smad3 pathway in cardiac fibroblasts of obese rats. Conclusions The paracrine effect of EAT-derived leptin on myocardial remodeling, inducing MMPs/TIMPs imbalance and promoting the proliferation of cardiac fibroblasts via activating ERK1/2 and JAK2/STAT3-TGF-β1/Smad3 pathway in obesity. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): the Nature Science Foundation of China (grant no. 81873513, 81600574, and 30871042)

scholarly journals Osthole Regulates TGF-β1 and MMP-2/9 Expressions via Activation of PPARα/γ in Cultured Mouse Cardiac Fibroblasts Stimulated with Angiotensin II

2013 ◽  
Vol 16 (5) ◽  
pp. 732 ◽  
Author(s):  
Rong Chen ◽  
Jie Xue ◽  
Meilin Xie
Keyword(s):  
Angiotensin Ii ◽  
Myocardial Fibrosis ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Underlying Mechanism ◽  
Nuclear Factor Κb ◽  
Peroxisome Proliferator ◽  
Active Constituent ◽  
Peroxisome Proliferator Activated Receptor ◽  
Tgf Β1

PURPOSE. Our previous studies have demonstrated that osthole, an active constituent isolated from the fruit of Cnidium monnieri (L.) Cusson, can prevent isoprenaline-induced myocardial fibrosis in mice, but the underlying mechanism is still unclear.  METHODS. The mouse cardiac fibroblasts (CFs) stimulated with angiotensin II (Ang II) were cultured and treated with different concentrations of osthole. The mRNA expressions of peroxisome proliferator-activated receptor (PPAR) α/γ, transforming growth factor β1 (TGF-β1), and matrix metalloproteinase (MMP)-2/9 were detected by reverse transcription polymerase chain reaction method, and the protein expressions of nuclear factor-κB (NF-κB) and TGF-β1 were detected by Western blot method, respectively.  RESULTS. Following treatment of cells with osthole at 2.5, 5, 10 and 20 μg/mL, the NF-κB and TGF-β1 expressions were dose-dependently decreased, while the expressions of PPARα/γ and MMP-2/9 were dose-dependently increased. After the cells were preincubated with PPARα antagonist (MK886) or/and PPARγ antagonist (GW9662), the inhibitions of osthole on the NF-κB and TGF-β1 expressions were decreased or completely halted and the increment of osthole on the MMP-2/9 expressions were also decreased or completely cancelled.  CONCLUSION. Osthole could inhibit the NF-κB and TGF-β1 expressions by activation of PPARα/γ, and subsequently enhance the MMP-2/9 expressions in cultured CFs, and these effects of osthole may play the beneficial roles in the prevention and treatment of myocardial fibrosis. This article is open to POST-PUBLICATION REVIEW.  Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page. 

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