scholarly journals The aortic ring model of angiogenesis: a quarter century of search and discovery

2009 ◽  
Vol 13 (10) ◽  
pp. 4113-4136 ◽  
Author(s):  
R. F. Nicosia
Keyword(s):  
Aortic Ring ◽  
Quarter Century ◽  
Ring Model

Rat Aortic Ring Model to Assay Angiogenesis ex vivo

BIO-PROTOCOL ◽  
2015 ◽  
Vol 5 (20) ◽  
Author(s):  
Isabelle Ernens ◽  
B�n�dicte Lenoir ◽  
Yvan Devaux ◽  
Daniel Wagner
Keyword(s):  
Ex Vivo ◽  
Aortic Ring ◽  
Ring Model ◽  
Rat Aortic Ring Model

scholarly journals 4-Pyridinio-1,4-Dihydropyridines as Calcium Ion Transport Modulators: Antagonist, Agonist, and Dual Action

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ilona Domracheva ◽  
Iveta Kanepe-Lapsa ◽  
Reinis Vilskersts ◽  
Imanta Bruvere ◽  
Egils Bisenieks ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neuroblastoma Cell ◽  
Aortic Ring ◽  
Antagonistic Effect ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Ring Model ◽  
A7r5 Cells ◽  
Intracellular Ca ◽  
The Impact

A set of six new 4-pyridinio-1,4-dihydropyridine (1,4-DHP) compounds has been synthesized. The calcium channel modulating activity of these compounds was evaluated in an aorta vascular smooth muscle cell line (A7R5), in an isolated rat aortic ring model, and in human neuroblastoma cell lines (SH-SY5Y). The antagonistic effect of these 1,4-DHP was tested by modulating the impact of carbachol-dependent mobilization of intracellular Ca2+ in SH-SY5Y cells. The intracellular free Ca2+ concentration was measured in confluent monolayers of SH-SY5Y cells and A7R5 cells with the Ca2+-sensitive fluorescent indicator Fluo-4 NW. Only four compounds showed calcium channel blocking activity in SH-SY5Y and A7R5 cells as well as in the aortic ring model. Among them, compound 3 was the most active calcium channel antagonist, which had 3 times higher activity on carbachol-activated SH-SY5Y cells than amlodipine. Two of the compounds were inactive. Compound 4 had 9 times higher calcium agonist activity than the classic DHP calcium agonist Bay K8644. The intracellular mechanism for the action of compound 4 using inhibitor analysis was elucidated. Nicotinic as well as muscarinic receptors were not involved. Sarcoplasmic reticulum (ER) Ca2+ (SERCA) stores were not affected. Ryanodine receptors (RyRs), another class of intracellular Ca2+ releasing channels, participated in the agonist response evoked by compound 4. The electrooxidation data suggest that the studied compounds could serve as antioxidants in OS.

scholarly journals Vascular regression and survival are differentially regulated by MT1-MMP and TIMPs in the aortic ring model of angiogenesis

2009 ◽  
Vol 297 (2) ◽  
pp. C471-C480 ◽  
Author(s):  
A. C. Aplin ◽  
W. H. Zhu ◽  
E. Fogel ◽  
R. F. Nicosia
Keyword(s):  
Inhibitory Activity ◽  
Neutralizing Antibodies ◽  
Critical Role ◽  
Collagen Gel ◽  
Aortic Ring ◽  
Aminocaproic Acid ◽  
Antiangiogenic Effect ◽  
Ring Model ◽  
The Matrix ◽  
Vascular Proliferation

This study was designed to investigate the role of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) in the reabsorption of neovessels in collagen gel cultures of rat and mouse aortic rings. Aortic angiogenesis was associated with collagen lysis and production of the matrix-degrading enzymes MMP-2, MMP-9, and membrane-type MMP (MT1-MMP, or MMP-14). Vascular growth and regression were not affected by disruption of MMP-2 or MMP-9. In addition, no effect on vascular regression was observed by blocking plasmin, a protease implicated in the activation of MMPs, with ε-aminocaproic acid or by adding plasminogen, which caused a modest increase in vascular proliferation. Conversely, angiogenesis was blocked and vessels stabilized by inhibiting MT1-MMP with neutralizing antibodies, TIMP-2, TIMP-3, or TIMP-4. TIMP-1, which blocks MMP-2 and MMP-9 but is a poor inhibitor of MT1-MMP, had no antiangiogenic effect. However, TIMP-1 prolonged the survival of neovessels following angiogenesis. Vascular regression was accelerated in aortic cultures from TIMP-1- and TIMP-2-deficient mice. The vascular survival effect of anti-MT1-MMP antibodies and TIMPs with MT1-MMP inhibitory activity was associated with complete inhibition of collagen lysis. In contrast, TIMP-1 had no anticollagenolytic effect. These results indicate that MT1-MMP plays a critical role not only in angiogenesis but also in vascular regression and demonstrate that TIMPs with anti-MT1-MMP activity have opposite effects on angiogenic outcomes depending on the stage of the angiogenic process. This study also suggests the existence of a TIMP-1-mediated alternate pathway of vascular survival that is unrelated to MT1-MMP inhibitory activity.

scholarly journals Purified Anthocyanin Supplementation Improves Endothelial Function via NO-cGMP Activation in Hypercholesterolemic Individuals

2011 ◽  
Vol 57 (11) ◽  
pp. 1524-1533 ◽  
Author(s):  
Yanna Zhu ◽  
Min Xia ◽  
Yan Yang ◽  
Fengqiong Liu ◽  
Zhongxia Li ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Hdl Cholesterol ◽  
Aortic Ring ◽  
Control Group ◽  
Short Term ◽  
Beneficial Effects ◽  
Ring Model ◽  
Vascular Adhesion ◽  
Rat Aortic Ring Model

BACKGROUND Anthocyanins have been shown to improve endothelial function in animal models. However, whether these compounds have similar beneficial effects in humans is largely unknown. METHODS In a short-term crossover study, 12 hypercholesterolemic individuals were given oral anthocyanins (320 mg) isolated from berries or placebo. Brachial artery flow-mediated dilation (FMD) was assessed before and after the intervention. In a long-term intervention trial (12 weeks), 150 hypercholesterolemic individuals were given anthocyanins (320 mg/day, n = 75) or placebo (n = 75), after which we measured FMD, plasma cGMP, and other serum biomarkers. Another short-term intervention was conducted in the presence of NO-cGMP inhibitors in 6 people and in a rat aortic ring model (n = 8). RESULTS Significant increases of FMD from 8.3% (0.6%) at baseline to 11.0% (0.8%) at 1 h and 10.1% (0.9%) at 2 h were observed after short-term anthocyanin consumption, concomitantly with increases of plasma anthocyanin concentrations (P < 0.05). In the study participants who received long-term anthocyanin intervention, compared with the control group, we observed significant increases in the FMD (28.4% vs 2.2%), cGMP (12.6% vs −1.2%), and HDL-cholesterol concentrations, but decreases in the serum soluble vascular adhesion molecule-1 and LDL cholesterol concentrations (P < 0.05). The changes in the cGMP and HDL cholesterol concentrations positively correlated with FMD in the anthocyanin group (P < 0.05). In the presence of NO-cGMP inhibitors, the effects of anthocyanin on endothelial function were abolished in human participants and in a rat aortic ring model. CONCLUSIONS Anthocyanin supplementation improves endothelium-dependent vasodilation in hypercholesterolemic individuals. This effect involves activation of the NO-cGMP signaling pathway, improvements in the serum lipid profile, and decreased inflammation.

Chapter 7 The Aortic Ring Model of Angiogenesis

2008 ◽  
pp. 119-136 ◽  
Author(s):  
Alfred C. Aplin ◽  
Eric Fogel ◽  
Penelope Zorzi ◽  
Roberto F. Nicosia
Keyword(s):  
Aortic Ring ◽  
Ring Model

scholarly journals B. anthracisedema toxin increases cAMP levels and inhibits phenylephrine-stimulated contraction in a rat aortic ring model

2013 ◽  
Vol 305 (2) ◽  
pp. H238-H250 ◽  
Author(s):  
Yan Li ◽  
Xizhong Cui ◽  
Steven B. Solomon ◽  
Kenneth Remy ◽  
Yvonne Fitz ◽  
...  
Keyword(s):  
Protective Antigen ◽  
Lethal Factor ◽  
Aortic Ring ◽  
Contractile Force ◽  
Host Cells ◽  
Sprague Dawley ◽  
Adenyl Cyclase Activity ◽  
Ring Model ◽  
Arterial Relaxation ◽  
Rat Aortic Ring Model

B. anthracis edema toxin (ET) and lethal toxin (LT) are each composed of protective antigen (PA), necessary for toxin uptake by host cells, and their respective toxic moieties, edema factor (EF) and lethal factor (LF). Although both toxins likely contribute to shock during infection, their mechanisms are unclear. To test whether ET and LT produce arterial relaxation, their effects on phenylephrine (PE)-stimulated contraction in a Sprague-Dawley rat aortic ring model were measured. Rings were prepared and connected to pressure transducers. Their viability was confirmed, and peak contraction with 60 mM KCl was determined. Compared with PA pretreatment (control, 60 min), ET pretreatment at concentrations similar to those noted in vivo decreased the mean (±SE) maximum contractile force (MCF; percent peak contraction) in rings generated during stimulation with increasing PE concentrations (96.2 ± 7.0 vs. 57.3 ± 9.1) and increased the estimated PE concentration producing half the MCF (EC50; 10−7M, 1.1 ± 0.3 vs. 3.7 ± 0.8, P ≤ 0.002). ET inhibition with PA-directed monoclonal antibodies, selective EF inhibition with adefovir, or removal of the ring endothelium inhibited the effects of ET on MCF and EC50( P ≤ 0.02). Consistent with its adenyl cyclase activity, ET increased tissue cAMP in endothelium-intact but not endothelium-denuded rings ( P < 0.0001 and 0.25, respectively). LT pretreatment, even in high concentrations, did not significantly decrease MCF or increase EC50(all P > 0.05). In rings precontracted with PE compared with posttreatment with PA (90 min), ET posttreatment produced progressive reductions in contractile force and increases in relaxation in endothelium-intact rings ( P < 0.0001) but not endothelium-denuded rings ( P = 0.51). Thus, ET may contribute to shock by producing arterial relaxation.

scholarly journals Interleukin-19 induces angiogenesis in the absence of hypoxia by direct and indirect immune mechanisms

2016 ◽  
Vol 310 (11) ◽  
pp. C931-C941 ◽  
Author(s):  
Farah Kako ◽  
Khatuna Gabunia ◽  
Mitali Ray ◽  
Sheri E. Kelemen ◽  
Ross N. England ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Aortic Ring ◽  
Peroxisome Proliferator ◽  
Wild Type ◽  
Rt Pcr ◽  
Screening Assay ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pcr Screening ◽  
Ring Model

Neovascularization and inflammation are independent biological processes but are linked in response to injury. The role of inflammation-dampening cytokines in the regulation of angiogenesis remains to be clarified. The purpose of this work was to test the hypothesis that IL-19 can induce angiogenesis in the absence of tissue hypoxia and to identify potential mechanisms. Using the aortic ring model of angiogenesis, we found significantly reduced sprouting capacity in aortic rings from IL-19−/−compared with wild-type mice. Using an in vivo assay, we found that IL-19−/−mice respond to vascular endothelial growth factor (VEGF) significantly less than wild-type mice and demonstrate decreased capillary formation in Matrigel plugs. IL-19 signals through the IL-20 receptor complex, and IL-19 induces IL-20 receptor subunit expression in aortic rings and cultured human vascular smooth muscle cells, but not endothelial cells, in a peroxisome proliferator-activated receptor-γ-dependent mechanism. IL-19 activates STAT3, and IL-19 angiogenic activity in aortic rings is STAT3-dependent. Using a quantitative RT-PCR screening assay, we determined that IL-19 has direct proangiogenic effects on aortic rings by inducing angiogenic gene expression. M2 macrophages participate in angiogenesis, and IL-19 has indirect angiogenic effects, as IL-19-stimulated bone marrow-derived macrophages secrete proangiogenic factors that induce greater sprouting of aortic rings than unstimulated controls. Using a quantitative RT-PCR screen, we determined that IL-19 induces expression of angiogenic cytokines in bone marrow-derived macrophages. Together, these data suggest that IL-19 can promote angiogenesis in the absence of hypoxia by at least two distinct mechanisms: 1) direct effects on vascular cells and 2) indirect effects by stimulation of macrophages.

Sign in / Sign up

Export Citation Format

Share Document