Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Lijnen, Paul

doi:10.2174/1876526201104010001

Cited by 7 publications

(7 citation statements)

References 178 publications

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“…Consistent with the previous studies (Chen et al, ; Yang et al, ; Lijnen, ), in the present experiment, we found that the expression of MMP‐1 was reduced but expressions of TIMP‐1 and TGF‐β1 were increased by Ang II. In addition, we found for the first time that levels of MMP‐1 could be increased ( in vitro and in vivo ) but TIMP‐1 ( in vitro ) and TGF‐β1 ( in vitro and in vivo ) could be decreased by pre‐miR‐214 treatment, and these effects were blocked almost completely by anti‐miR‐214 treatment.…”

Section: Discussionsupporting

confidence: 93%

“…Also, we chose a relatively lower concentration of Ang II, which may cause nearly 50% increased cell vitality. Similar findings have also been described by Lijnen et al (Li et al, ; Lijnen, ).…”

Section: Discussionsupporting

confidence: 91%

“…AMI may activate renin‐angiotensin‐aldosterone system, leading to increased level of Ang II, which may consequently increase TGF‐β1 and reactive oxygen species (ROS), contributing to fibrosis progress (Chen et al, ; Yang et al, ; Creemers and Pinto, ; Lijnen, ; Lijnen et al, ). Previous studies indicate that ROS may increase the expression of COL I, TIMP‐1 and decrease the activity and expression of MMP‐1 through the ROS‐sensitive transcription factors nuclear factor κ B (NF‐ κ B) and/or activator protein‐1 (AP‐1) (Chen et al, ; Yang et al, ; Lijnen PJ, ; Lijnen et al, ). Inhibition of ROS by Pioglitazone (Chen et al, ) and Tempo (Lijnen et al, ) may attenuate the effects of Ang II.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

Hua

Dong

Zhang

et al. 2016

The Anatomical Record

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The miRNAs play important roles in regulating myocardial fibrosis. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in cardiac fibrosis in vitro and in vivo. In vitro experiment, Ang II-induced cardiac fibroblasts (CFBs) are transfected with pre-miR-214, anti-miR-214 and their oligo controls. Gene expression was checked by Quantitative realtime-PCR (qRT-PCR) and western blotting. In the present experiment, compared with controls, expressions of collagen type I (COL I), collagen type III (COL III), transforming growth factor (TGF)-β1, and tissue inhibitors of metalloproteinase (TIMP)-1 were all increased, but matrix metalloproteinase (MMP)-1 was reduced in CFB by Ang II treatment at both mRNA and protein levels, and these alterations were found reversed by miR-214 transfection. In vivo, an anterior transmural acute myocardial infarction (AMI) was created by occlusion of the left anterior descending coronary artery after Ad-pre-miR-214, Ad-anti-miR-214 or Ad-GFP was delivered separately. Four weeks after AMI, protein contents of COL I, COL III and TGF-β1 in tissue from border area were found increased after AMI, but impaired by overexpression of miR-214. While the expression of MMP-1 was increased by miR-214 stimulation but decreased by miR-214 inhibition. These results suggested that miR-214 exerts cardio-protective effects by inhibition of fibrosis and the inhibitory effect involves TGF-β1 suppression and MMP-1/TIMP-1 regulation. Anat Rec, 299:1348-1357, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

Hua

Dong

Zhang

et al. 2016

The Anatomical Record

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“…In previous studies [40,41], Ang II has been shown to increase collagen synthesis. In previous studies [40,41], Ang II has been shown to increase collagen synthesis.…”

Section: Discussionmentioning

confidence: 85%

Cyclic Pressure and Angiotensin II Influence the Biomechanical Properties of Aortic Valves

Myles¹,

Liao²,

Warnock

2013

Journal of Biomechanical Engineering

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Hypertension is a known risk factor for aortic stenosis. The elevated blood pressure increases the transvalvular load and can elicit inflammation and extracellular matrix (ECM) remodeling. Elevated cyclic pressure and the vasoactive agent angiotensin II (Ang II) both promote collagen synthesis, an early hallmark of aortic sclerosis. In the current study, it was hypothesized that elevated cyclic pressure and/or angiotensin II decreases extensibility of aortic valve leaflets due to an increase in collagen content and/or interstitial cell stiffness. Porcine aortic valve leaflets were exposed to pressure conditions of increasing magnitude (static atmospheric pressure, 80, and 120 mmHg) with and without 10−6 M Ang II. Biaxial mechanical testing was performed to determine extensibility in the circumferential and radial directions and collagen content was determined using a quantitative dye-binding method at 24 and 48 h. Isolated aortic valve interstitial cells exposed to the same experimental conditions were subjected to atomic force microscopy to assess cellular stiffness at 24 h. Leaflet tissue incubated with Ang II decreased tissue extensibility in the radial direction, but not in the circumferential direction. Elevated cyclic pressure decreased extensibility in both the radial and circumferential directions. Ang II and elevated cyclic pressure both increased the collagen content in leaflet tissue. Interstitial cells incubated with Ang II were stiffer than those incubated without Ang II while elevated cyclic pressure caused a decrease in cell stiffness. The results of the current study demonstrated that both pressure and Ang II play a role in altering the biomechanical properties of aortic valve leaflets. Ang II and elevated cyclic pressure decreased the extensibility of aortic valve leaflet tissue. Ang II induced direction specific changes in extensibility, demonstrating different response mechanisms. These findings help to provide a better understanding of the responses of aortic valves to mechanical and biochemical changes that occur under hypertensive conditions.

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“…Increased collagen deposition may be due to oxidative stress that stimulates the expression of genes involved in collagen biosynthesis (Guler et al, 2009). Moreover, inhibition of superoxide dismutase (antioxidant enzyme) stimulates collagen production and this demonstrated a vital role of superoxide dismutase and the generated reactive oxygen species (ROS) in collagen accumulation (Lijnen et al, 2011). Results of the current study revealed increased PAS +ve materials in the thickened walls of bronchioles, arteries and alveolar septae with moderately stained granuloma areas in lungs of pregnant rats of groups S1, S2 and revealed decreased PAS +ve materials in the fetuses of S1, S2 groups in a dose dependent manner as compared to control group.…”

Section: Journal Of Biology and Life Sciencementioning

confidence: 99%

Maternal and Fetal Toxicity of Carisoprodol Drug (Somadril Compound) on Pulmonary Tissues of Albino Rats

Emam

2019

JBLS

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Carisoprodol is a common muscle relaxant indicated as adjunctive therapy in acute, painful musculoskeletal cases. This current study aimed to investigate the histopathological, histochemical and immunohistochemical effects in the lung tissue of the pregnant rats and their fetuses after carisoprodol treatment. The present study was applied on twenty seven pregnant female rats and they were randomly divided into three groups (nine pregnant female rats in each group). Rats of the first (control) group were administered oral doses of distilled water. Rats of the second (S1) and third groups (S2) were administered oral doses of carisoprodol in the distilled water equivalent to 10.8 mg and 21.6 mg/100g body weight/day respectively for fifteen days from the six to the twenty day of gestation. Several histopathological, histochemical and some immunohistochemical changes were studied to detect the pathological changes. Maternal and fetal pulmonary tissues of both treated groups showed numerous degenerative changes post-treatment with carisoprodol, the severity of these changes was more obvious in the fetal lung tissue of both groups. Also, carisoprodol treated rats showed a marked increase in caspase-3 content in the maternal and fetal pulmonary tissues. Treatment of pregnant rats with carisoprodol drug led to numerous dystrophic changes in both maternal and fetal lung tissues.

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Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Cited by 7 publications

References 178 publications

MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

Cyclic Pressure and Angiotensin II Influence the Biomechanical Properties of Aortic Valves

Maternal and Fetal Toxicity of Carisoprodol Drug (Somadril Compound) on Pulmonary Tissues of Albino Rats

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