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 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 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 ERK and p38 MAPK, but not NF-κB, Are Critically Involved in Reactive Oxygen Species–Mediated Induction of IL-6 by Angiotensin II in Cardiac Fibroblasts

2001 ◽  
Vol 89 (8) ◽  
pp. 661-669 ◽  
Author(s):  
Motoaki Sano ◽  
Keiichi Fukuda ◽  
Toshihiko Sato ◽  
Haruko Kawaguchi ◽  
Makoto Suematsu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
P38 Mapk ◽  
Cardiac Fibroblasts ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Angiotensin II upregulates fibroblast-myofibroblast transition through Cx43-dependent CaMKII and TGF-β1 signaling in neonatal rat cardiac fibroblasts

2018 ◽  
Vol 50 (9) ◽  
pp. 843-852 ◽  
Author(s):  
Li Cao ◽  
Yunlin Chen ◽  
Li Lu ◽  
Yihao Liu ◽  
Yaowen Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblasts ◽  
Neonatal Rat ◽  
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 TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways

2007 ◽  
Vol 293 (3) ◽  
pp. L790-L799 ◽  
Author(s):  
Mickey M. Martin ◽  
Jessica A. Buckenberger ◽  
Jinmai Jiang ◽  
Geraldine E. Malana ◽  
Daren L. Knoell ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Pulmonary Fibrosis ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Lung Fibroblasts ◽  
Pi3k Signaling ◽  
R Gene ◽  
Ang Ii ◽  
Tgf Β1

Both angiotensin II (ANG II) and transforming growth factor-β1 (TGF-β1) are thought to be involved in mediating pulmonary fibrosis. Interactions between the renin-angiotensin system (RAS) and TGF-β1 have been well documented, with most studies describing the effect of ANG II on TGF-β1 expression. However, recent gene expression profiling experiments demonstrated that the angiotensin II type 1 receptor (AT1R) gene was a novel TGF-β1 target in human adult lung fibroblasts. In this report, we show that TGF-β1 augments human AT1R (hAT1R) steady-state mRNA and protein levels in a dose- and time-dependent manner in primary human fetal pulmonary fibroblasts (hPFBs). Nuclear run-on experiments demonstrate that TGF-β1 transcriptionally activates the hAT1R gene and does not influence hAT1R mRNA stability. Pharmacological inhibitors and specific siRNA knockdown experiments demonstrate that the TGF-β1 type 1 receptor (TβRI/ALK5), Smad2/3, and Smad4 are essential for TGF-β1-stimulated hAT1R expression. Additional pharmacological inhibitor and small interference RNA experiments also demonstrated that p38 MAPK, JNK, and phosphatidylinositol 3-kinase (PI3K) signaling pathways are also involved in the TGF-β1-stimulated increase in hAT1R density. Together, our results suggest an important role for cross talk among Smad, p38 MAPK, JNK, and PI3K pathways in mediating the augmented expression of hAT1R following TGF-β1 treatment in hPFB. This study supports the hypothesis that a self-potentiating loop exists between the RAS and the TGF-β1 signaling pathways and suggests that ANG II and TGF-β1 may cooperate in the pathogenesis of pulmonary fibrosis. The synergy between these systems may require that both pathways be simultaneously inhibited to treat fibrotic lung disease.

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)

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