scholarly journals Histone deacetyltransferase inhibitors Trichostatin A and Mocetinostat differentially regulate MMP9, IL-18 and RECK expression, and attenuate Angiotensin II-induced cardiac fibroblast migration and proliferation

2016 ◽  
Vol 39 (10) ◽  
pp. 709-716 ◽  
Author(s):  
Naveen K Somanna ◽  
Anthony J Valente ◽  
Maike Krenz ◽  
Kerry S McDonald ◽  
Yusuke Higashi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Trichostatin A ◽  
Cardiac Fibroblast ◽  
Fibroblast Migration ◽  
Histone Deacetyltransferase

scholarly journals Angiotensin II stimulates cardiac fibroblast migration via the differential regulation of matrixins and RECK

2013 ◽  
Vol 65 ◽  
pp. 9-18 ◽  
Author(s):  
Jalahalli M. Siddesha ◽  
Anthony J. Valente ◽  
Siva S.V.P. Sakamuri ◽  
Tadashi Yoshida ◽  
Jason D. Gardner ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Differential Regulation ◽  
Cardiac Fibroblast ◽  
Fibroblast Migration

scholarly journals Docosahexaenoic acid reverses angiotensin II-induced RECK suppression and cardiac fibroblast migration

2014 ◽  
Vol 26 (5) ◽  
pp. 933-941 ◽  
Author(s):  
Jalahalli M. Siddesha ◽  
Anthony J. Valente ◽  
Tadashi Yoshida ◽  
Siva S.V.P. Sakamuri ◽  
Patrice Delafontaine ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Docosahexaenoic Acid ◽  
Cardiac Fibroblast ◽  
Fibroblast Migration

scholarly journals Sodium Tanshinone IIA Sulfonate Prevents Angiotensin II-Induced Differentiation of Human Atrial Fibroblasts into Myofibroblasts

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Tangting Chen ◽  
Miaoling Li ◽  
Xuehui Fan ◽  
Jun Cheng ◽  
Liqun Wang
Keyword(s):  
Angiotensin Ii ◽  
Critical Role ◽  
Water Soluble ◽  
Collagen I ◽  
Tanshinone Iia ◽  
Ang Ii ◽  
Induced Differentiation ◽  
Fibroblast Migration ◽  
Collagen Iii ◽  
Sodium Tanshinone Iia Sulfonate

Differentiation of atrial fibroblasts into myofibroblasts plays a critical role in atrial fibrosis. Sodium tanshinone IIA sulfonate (DS-201), a water-soluble derivative of tanshinone IIA, has been shown to have potent antifibrotic properties. However, the protective effects of DS-201 on angiotensin II- (Ang II-) induced differentiation of atrial fibroblasts into myofibroblasts remain to be elucidated. In this study, human atrial fibroblasts were stimulated with Ang II in the presence or absence of DS-201. Then, α-smooth muscle actin (α-SMA), collagen I, and collagen III expression and reactive oxygen species (ROS) generation were measured. The expression of transforming growth factor-β1 (TGF-β1) and the downstream signaling of TGF-β1, such as phosphorylation of Smad2/3, were also determined. The results demonstrated that DS-201 significantly prevented Ang II-induced human atrial fibroblast migration and decreased Ang II-induced α-SMA, collagen I, and collagen III expression. Furthermore, increased production of ROS and expression of TGF-β1 stimulated by Ang II were also significantly inhibited by DS-201. Consistent with these results, DS-201 significantly inhibited Ang II-evoked Smad2/3 phosphorylation and periostin expression. These results and the experiments involving N-acetyl cysteine (antioxidant) and an anti-TGF-β1 antibody suggest that DS-201 prevent Ang II-induced differentiation of atrial fibroblasts to myofibroblasts, at least in part, through suppressing oxidative stress and inhibiting the activation of TGF-β1 signaling pathway. All of these data indicate the potential utility of DS-201 for the treatment of cardiac fibrosis.

scholarly journals MicroRNA‑144 regulates angiotensin II‑induced cardiac fibroblast activation by targeting CREB

2020 ◽  
Author(s):  
Zhi‑Yong Liu ◽  
Mingjun Lu ◽  
Jing Liu ◽  
Zhao‑Ning Wang ◽  
Wei‑Wei Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblast ◽  
Fibroblast Activation

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.

223 ADRENERGIC REGULATION OF CARDIAC FIBROBLAST MIGRATION.

2004 ◽  
Vol 52 (Suppl 1) ◽  
pp. S118.2-S118
Author(s):  
R. E. Laird ◽  
M. D. Mitchell ◽  
R. D. Brown ◽  
C. S. Long
Keyword(s):  
Cardiac Fibroblast ◽  
Adrenergic Regulation ◽  
Fibroblast Migration

Angiotensin II modulates nitric oxide-induced cardiac fibroblast apoptosis by activation of AKT/PKB

2003 ◽  
Vol 285 (3) ◽  
pp. H1105-H1112 ◽  
Author(s):  
Bin Tian ◽  
Jian Liu ◽  
Peter Bitterman ◽  
Robert J. Bache
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Cardiac Fibroblast ◽  
Inos Expression ◽  
No Production ◽  
Ang Ii ◽  
Phosphatidylinositol 3 Kinase ◽  
No Donor ◽  
At1 Antagonist ◽  
Phosphatidylinositol 3

Previously we found that interleukin-1β (IL-1β)-activated inducible nitric oxide (NO) synthase (iNOS) expression and that NO production can trigger cardiac fibroblast (CFb) apoptosis. Here, we provide evidence that angiotensin II (ANG II) significantly attenuated IL-1β-induced iNOS expression and NO production in CFbs while simultaneously decreasing apoptotic frequency. The anti-apoptotic effect of ANG II was abolished when cells were pretreated with the specific ANG II type 1 receptor (AT1) antagonist losartan, but not by the AT2 antagonist DP-123319. Furthermore, ANG II also protected CFbs from apoptosis induced by the NO donor diethylenetriamine NONOate and this effect was associated with phosphorylation of Akt/protein kinase B at Ser473. The effects of ANG II on Akt phosphorylation and NO donor-induced CFb apoptosis were abrogated when cells were preincubated with the specific phosphatidylinositol 3-kinase inhibitors wortmannin or LY-294002. These data demonstrate that ANG II protection of CFbs from IL-1β-induced apoptosis is associated with downregulation of iNOS expression and requires an intact phosphatidylinositol 3-kinase-Akt survival signal pathway. The findings suggest that ANG II and NO may play a role in regulating the cell population size by their countervailing influences on cardiac fibroblast viability.

ISH NIA PS 01-03 Trichostatin A Inhibits Angiotensin II-induced Hypertension Via p66shc Dephosphorylation

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e275
Author(s):  
Yu Ran LEE ◽  
Gun Kang ◽  
Hee Kyoung Joo ◽  
Myoung Soo Park ◽  
Cuk-Seong Kim ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Trichostatin A ◽  
Induced Hypertension

scholarly journals Expression of fibulin-6 in failing hearts and its role for cardiac fibroblast migration

2014 ◽  
Vol 103 (4) ◽  
pp. 509-520 ◽  
Author(s):  
Arpita Chowdhury ◽  
Christine Herzog ◽  
Lisa Hasselbach ◽  
Houra Loghmani Khouzani ◽  
Jinli Zhang ◽  
...  
Keyword(s):  
Cardiac Fibroblast ◽  
Fibroblast Migration
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