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Journal articles on the topic 'Neointimal growth'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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1

Matsuda, Yoshikazu, Joonho Chung, and Demetrius K. Lopes. "Analysis of neointima development in flow diverters using optical coherence tomography imaging." Journal of NeuroInterventional Surgery 10, no. 2 (2017): 162–67. http://dx.doi.org/10.1136/neurintsurg-2016-012969.

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BackgroundFlow diverters are used for the treatment of intracranial aneurysms. Surface modification may decrease the thrombogenicity of flow diverters but the details are unknown. Optical coherence tomography (OCT) is an intravascular imaging test with high resolution which identifies neointimal growth over stents. We compared the development of neointima in a flow diverter and stents with and without surface modification in a swine model.MethodsIn this study we implanted four devices (two in each carotid artery) in four pigs. The devices used were the Pipeline Flex embolization device (PED Fl

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Yang, Jian, Yunhui Cheng, Ruirui Ji, and Chunxiang Zhang. "Novel model of inflammatory neointima formation reveals a potential role of myeloperoxidase in neointimal hyperplasia." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (2006): H3087—H3093. http://dx.doi.org/10.1152/ajpheart.00412.2006.

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Atherosclerosis, which is characterized by neointima formation, is an inflammatory disease. However, there is no inflammatory product-elicited neointimal model to support the causal role of inflammation in atherogenesis. We reported previously that leukocyte-derived MPO induces vascular injury responses such as endothelial dysfunction. We now test the role of MPO in inflammatory neointima formation. We infused temporarily isolated rat common carotid arteries with MPO (200 nM) and incubated for 1 h. We found that although MPO itself did not induce any neointima formation 2 wk after treatment, i

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3

Dale, William E., and Edward H. Blaine. "Effects of enalaprilat on neointimal growth of cultured rabbit aorta following balloon injury." Canadian Journal of Physiology and Pharmacology 77, no. 10 (1999): 763–69. http://dx.doi.org/10.1139/y99-062.

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Our objective was to determine if the ability of an angiotensin-converting enzyme (ACE) inhibitor to attenuate neointima formation in balloon-damaged vessel is expressed in an isolated organ culture model of neointimal growth. In vivo balloon angioplasty in combination with in vitro organ culture was used to produce a unique model of vascular neointima formation. Aortic segments were cultured in medium containing a broad concentration range of the ACE inhibitor enalaprilat (0-100 µM). Cell proliferative indices and neointima:media thickness ratios were determined from vessel segments after 1,

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Asada, Yujiro, Seiichiro Hara, Atsushi Tsuneyoshi, et al. "Fibrin-Rich and Platelet-Rich Thrombus Formation on Neointima: Recombinant Tissue Factor Pathway Inhibitor Prevents Fibrin Formation and Neointimal Development following Repeated Balloon Injury of Rabbit Aorta." Thrombosis and Haemostasis 80, no. 09 (1998): 506–11. http://dx.doi.org/10.1055/s-0037-1615237.

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SummaryThrombus formation and neointimal growth are the critical events in restenosis after balloon angioplasty. However, the responses of diseased vessels to injuries caused by balloon angioplasty have not been well examined. We investigated the thrombus formation and neointimal development following the balloon injury to the previously induced neointima in the rabbit aorta and the effects of recombinant tissue factor pathway inhibitor (rTFPI) on these responses. Rabbit thoracic aortas were subjected to injury with a Fogarty 4F balloon catheter at 1.75 atm (first injury), and 4 weeks later th

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Brown, J., Q. Chen, and G. Hong. "An autocrine system for C-type natriuretic peptide within rat carotid neointima during arterial repair." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2919—H2931. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2919.

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C-type natriuretic peptides (CNPs) are produced by endothelium and inhibit vascular smooth muscle cell (VSMC) proliferation. However, endothelial damage stimulates only transient VSMC proliferation in arteries. Here we report that a new source of CNP develops in rat carotid neointima 14 days after balloon angioplasty, when VSMC replication is subsiding despite continued absence of endothelium. CNP was detected immunohistochemically in neointimal but not medial VSMC. No other natriuretic peptides were detected immunohistochemically. CNP immunoreactivity (0.036 +/- 0.010 fmol/mg wet wt) was foun

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Mori, Yusaku, Marel Gonzalez Medina, Zhiwei Liu, et al. "Roles of vascular endothelial and smooth muscle cells in the vasculoprotective effect of insulin in a mouse model of restenosis." Diabetes and Vascular Disease Research 18, no. 3 (2021): 147916412110273. http://dx.doi.org/10.1177/14791641211027324.

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Background: Insulin exerts vasculoprotective effects on endothelial cells (ECs) and growth-promoting effects on vascular smooth muscle cells (SMCs) in vitro, and suppresses neointimal growth in vivo. Here we determined the role of ECs and SMCs in the effect of insulin on neointimal growth. Methods: Mice with transgene CreERT2 under the control of EC-specific Tie2 (Tie2-Cre) or SMC-specific smooth muscle myosin heavy chain promoter/enhancer (SMMHC-Cre) or littermate controls were crossbred with mice carrying a loxP-flanked insulin receptor (IR) gene. After CreERT2-loxP-mediated recombination wa

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7

Igura, Takumi, Sumio Kawata, Jun-ichiro Miyagawa, et al. "Expression of Heparin-Binding Epidermal Growth Factor–Like Growth Factor in Neointimal Cells Induced by Balloon Injury in Rat Carotid Arteries." Arteriosclerosis, Thrombosis, and Vascular Biology 16, no. 12 (1996): 1524–31. http://dx.doi.org/10.1161/01.atv.16.12.1524.

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Balloon catheter injury of rat carotid arteries induces migration and proliferation of smooth muscle cells (SMCs), with subsequent neointimal formation. Several growth factors, such as platelet-derived growth factor and basic fibroblast growth factor, have been shown to be involved in this process, but the mechanisms that modulate the growth and/or migratory properties of SMCs remain unclear. In this study, we investigated whether heparin-binding epidermal growth factor–like growth factor (HB-EGF), which is known to be a potent SMC stimulator from in vitro study, is associated with the prolife

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8

Yang, Di, Zhenghua Su, Gang Wei, et al. "H3K4 Methyltransferase Smyd3 Mediates Vascular Smooth Muscle Cell Proliferation, Migration, and Neointima Formation." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 6 (2021): 1901–14. http://dx.doi.org/10.1161/atvbaha.121.314689.

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Objective: Smyd3 (SET and MYND domain-containing protein 3) is an H3K4 (histone H3 lysine 4) dimethyltransferase and trimethyltransferase that activates the transcription of oncogenes and cell cycle genes in human cancer cells. We discovered its overexpression in proliferative vascular smooth muscle cells (VSMCs). However, whether Smyd3 plays a role in vascular remodeling remains unanswered. The objective of this study is to investigate the role and underlying mechanism of Smyd3 in phenotypic transition of VSMCs (such as proliferation and migration) and vascular remodeling (such as neointima f

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9

Pan, Chun-Hsu, Yu-Pei Lin, Jie-Yu Wang, et al. "Preventive Effect and Mechanism of Crossostephium chinense Extract on Balloon Angioplasty-Induced Neointimal Hyperplasia." Evidence-Based Complementary and Alternative Medicine 2021 (June 30, 2021): 1–11. http://dx.doi.org/10.1155/2021/8466543.

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Balloon angioplasty-induced neointimal hyperplasia remains a clinical problem that must be resolved. The bioactivities of the Crossostephium chinense extract (CCE) have demonstrated potential in preventing the progression of restenosis. The present study evaluated whether CCE can suppress balloon angioplasty-induced neointima formation and elucidated its possible pharmacological mechanisms. A rat model of carotid arterial balloon angioplasty was established to evaluate the inhibitory effect of CCEs on neointimal hyperplasia. Two cell lines, A10 vascular smooth muscle cells (VSMCs) and RAW264.7

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Matsuda, Yoshikazu, Dong-Kyu Jang, Joonho Chung, John Michael Wainwright, and Demetrius Lopes. "Preliminary outcomes of single antiplatelet therapy for surface-modified flow diverters in an animal model: analysis of neointimal development and thrombus formation using OCT." Journal of NeuroInterventional Surgery 11, no. 1 (2018): 74–79. http://dx.doi.org/10.1136/neurintsurg-2018-013935.

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ObjectiveTo evaluate the rate of neointimal development and thrombus formation of surface-modified flow diverters in single antiplatelet therapy (SAPT) using optical coherence tomography (OCT) in a porcine model.MethodsWe divided 10 experimental pigs into two groups. One group (n=6) received dual antiplatelet therapy (DAPT) and the other group (n=4) received SAPT. Four stents (two per carotid artery) were implanted in both groups. The stents used were the Pipeline Flex embolization device (PED Flex), Pipeline Flex with Shield technology (PED Shield), and the Solitaire AB stent. All animals und

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Zun, P. S., A. J. Narracott, C. Chiastra, J. Gunn, and A. G. Hoekstra. "Location-Specific Comparison Between a 3D In-Stent Restenosis Model and Micro-CT and Histology Data from Porcine In Vivo Experiments." Cardiovascular Engineering and Technology 10, no. 4 (2019): 568–82. http://dx.doi.org/10.1007/s13239-019-00431-4.

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Abstract Background Coronary artery restenosis is an important side effect of percutaneous coronary intervention. Computational models can be used to better understand this process. We report on an approach for validation of an in silico 3D model of in-stent restenosis in porcine coronary arteries and illustrate this approach by comparing the modelling results to in vivo data for 14 and 28 days post-stenting. Methods This multiscale model includes single-scale models for stent deployment, blood flow and tissue growth in the stented vessel, including smooth muscle cell (SMC) proliferation and e

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Jain, Manish, Nirav Dhanesha, Prakash Doddapattar, et al. "Smooth Muscle Cell–Specific PKM2 (Pyruvate Kinase Muscle 2) Promotes Smooth Muscle Cell Phenotypic Switching and Neointimal Hyperplasia." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 5 (2021): 1724–37. http://dx.doi.org/10.1161/atvbaha.121.316021.

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Objective: The role of glycolytic enzyme PKM2 (pyruvate kinase muscle 2) in smooth muscle cell (SMC) phenotype switching and neointimal hyperplasia is poorly understood. We determined the role of PKM2 in SMC phenotype switching and neointimal hyperplasia. Approach and Results: We show that PKM2 is expressed in the SMC-rich neointima of the murine carotid artery and peri-strut areas in bare-metal stented human coronary arteries. PDGF-BB (platelet-derived growth factor-BB) stimulation upregulates the expression of PKM2 in cultured murine and human coronary SMC. To provide conclusive evidence for

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Fontaine, Arthur B., Susan Dos Passos, Dimitrios Spigos, Jody Cearlock, and Alberto Urbaneja. "Use of Polyetherurethane to Improve the Biocompatibility of Vascular Stents." Journal of Endovascular Therapy 2, no. 3 (1995): 255–65. http://dx.doi.org/10.1177/152660289500200304.

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Purpose: To investigate potential differential growth of neointima following overdilating arterial trauma with polyetherurethane-coated versus bare metalìc stents in swine. Methods: Twelve specially constructed tantalum stents, 6 coated with polyetherurethane block copolymer and 6 uncoated, were overdilated by 25% in 12 normal renal arteries of six swine. The stents were harvested 8 weeks after implantation and prepared for histologic examination. Neointimal thickness was quantified and analyzed for significant differences between coated and uncoated prostheses. Results: All specimens demonstr

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Zhang, Chunxiang, Daniel L. Baker, Satoshi Yasuda та ін. "Lysophosphatidic Acid Induces Neointima Formation Through PPARγ Activation". Journal of Experimental Medicine 199, № 6 (2004): 763–74. http://dx.doi.org/10.1084/jem.20031619.

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Neointimal lesions are characterized by accumulation of cells within the arterial wall and are a prelude to atherosclerotic disease. Here we report that a brief exposure to either alkyl ether analogs of the growth factor–like phospholipid lysophosphatidic acid (LPA), products generated during the oxidative modification of low density lipoprotein, or to unsaturated acyl forms of LPA induce progressive formation of neointima in vivo in a rat carotid artery model. This effect is completely inhibited by the peroxisome proliferator-activated receptor (PPAR)γ antagonist GW9662 and mimicked by PPARγ

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Li, Fang, Chunxiang Zhang, Susan Schaefer, Anne Estes, and Kafait U. Malik. "ANG II-induced neointimal growth is mediated via cPLA2- and PLD2-activated Akt in balloon-injured rat carotid artery." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (2005): H2592—H2601. http://dx.doi.org/10.1152/ajpheart.00450.2005.

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Angiotensin II (ANG II) promotes neointimal growth in the balloon-injured rat carotid artery. However, the mechanism by which ANG II stimulates neointimal growth during vascular injury is not known. In cultured vascular smooth muscle cells, ANG II activates Akt through cytosolic phospholipase A2 (cPLA2)-dependent phospholipase D2 (PLD2). This study was conducted to determine whether ANG II-induced neointimal thickening is mediated via cPLA2- and PLD2-activated Akt in balloon-injured rat carotid arteries. ANG II-stimulated neointimal growth was inhibited by exposure of the injured carotid arter

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Hwang, Ae-Rang, Hee-Jung Lee, Suji Kim, Seong-Hee Park, and Chang-Hoon Woo. "Inhibition of p90RSK Ameliorates PDGF-BB-Mediated Phenotypic Change of Vascular Smooth Muscle Cell and Subsequent Hyperplasia of Neointima." International Journal of Molecular Sciences 24, no. 9 (2023): 8094. http://dx.doi.org/10.3390/ijms24098094.

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Platelet-derived growth factor type BB (PDGF-BB) regulates vascular smooth muscle cell (VSMC) migration and proliferation, which play critical roles in the development of vascular conditions. p90 ribosomal S6 kinase (p90RSK) can regulate various cellular processes through many different target substrates in several cell types, but the regulatory function of p90RSK on PDGF-BB-mediated cell migration and proliferation and subsequent vascular neointima formation has not yet been extensively examined. In this study, we investigated whether p90RSK inhibition protects VSMCs against PDGF-BB-induced c

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Wu, Qi, Yuanyang Chen, Zhiwei Wang, et al. "Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis." Oxidative Medicine and Cellular Longevity 2021 (December 3, 2021): 1–13. http://dx.doi.org/10.1155/2021/3119953.

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Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that ma

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Zernecke, Alma, and Andreas Schober. "Chemokines in vascular remodeling." Thrombosis and Haemostasis 97, no. 05 (2007): 730–37. http://dx.doi.org/10.1160/th07-02-0085.

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SummaryThe arterial vessel wall response to a variety of injuries consists in structural changes, which can result in luminal narrowing and aggravation of the underlying disease.This arterial remodeling is characterized by neointima formation and medial thickening, inflammatory cell recruitment and endothelial dysfunction. Chemokines and the corresponding receptors have been shown to participate at every step of the remodeling process.The monocyte chemotactic protein (MCP)-1/CC motif receptor 2 (CCR2) axis induces monocyte infiltration of the injured vessel wall and can stimulate proliferation

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Jeong, Kyuho, Jung-Hyun Kim, James M. Murphy, et al. "Nuclear Focal Adhesion Kinase Controls Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia Through GATA4-Mediated Cyclin D1 Transcription." Circulation Research 125, no. 2 (2019): 152–66. http://dx.doi.org/10.1161/circresaha.118.314344.

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Rationale: Neointimal hyperplasia is characterized by excessive accumulation of vascular smooth muscle cells (SMCs) leading to occlusive disorders, such as atherosclerosis and stenosis. Blood vessel injury increases growth factor secretion and matrix synthesis, which promotes SMC proliferation and neointimal hyperplasia via FAK (focal adhesion kinase). Objective: To understand the mechanism of FAK action in SMC proliferation and neointimal hyperplasia. Methods and Results: Using combined pharmacological FAK catalytic inhibition (VS-4718) and SMC-specific FAK kinase-dead (Myh11-Cre-ER T2 ) mous

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Farb, Andrew, Michael John, Eduardo Acampado, Frank D. Kolodgie, Margaret Forney Prescott, and Renu Virmani. "Oral Everolimus Inhibits In-Stent Neointimal Growth." Circulation 106, no. 18 (2002): 2379–84. http://dx.doi.org/10.1161/01.cir.0000033973.06059.04.

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Tahir, Hannan, Alfons G. Hoekstra, Eric Lorenz, et al. "Multi-scale simulations of the dynamics of in-stent restenosis: impact of stent deployment and design." Interface Focus 1, no. 3 (2011): 365–73. http://dx.doi.org/10.1098/rsfs.2010.0024.

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Neointimal hyperplasia, a process of smooth muscle cell re-growth, is the result of a natural wound healing response of the injured artery after stent deployment. Excessive neointimal hyperplasia following coronary artery stenting results in in-stent restenosis (ISR). Regardless of recent developments in the field of coronary stent design, ISR remains a significant complication of this interventional therapy. The influence of stent design parameters such as strut thickness, shape and the depth of strut deployment within the vessel wall on the severity of restenosis has already been highlighted

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Baeza, Ciro, Arancha Pintor-Chocano, Susana Carrasco, Ana Sanz, Alberto Ortiz, and Maria Dolores Sanchez-Niño. "Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia." International Journal of Molecular Sciences 25, no. 9 (2024): 4814. http://dx.doi.org/10.3390/ijms25094814.

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Neointimal hyperplasia is the main cause of vascular graft failure in the medium term. Vitamin D receptor activation modulates the biology of vascular smooth muscle cells and has been reported to protect from neointimal hyperplasia following endothelial injury. However, the molecular mechanisms are poorly understood. We have now explored the impact of the selective vitamin D receptor activator, paricalcitol, on neointimal hyperplasia, following guidewire-induced endothelial cell injury in rats, and we have assessed the impact of paricalcitol or vehicle on the expression of key cell stress fact

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Tahir, Hannan, Carles Bona-Casas, Andrew James Narracott, et al. "Endothelial repair process and its relevance to longitudinal neointimal tissue patterns: comparing histology with in silico modelling." Journal of The Royal Society Interface 11, no. 94 (2014): 20140022. http://dx.doi.org/10.1098/rsif.2014.0022.

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Re-establishing a functional endothelium following endovascular treatment is an important factor in arresting neointimal proliferation. In this study, both histology ( in vivo ) and computational simulations ( in silico ) are used to evaluate neointimal growth patterns within coronary arteries along the axial direction of the stent. Comparison of the growth configurations in vivo and in silico was undertaken to identify candidate mechanisms for endothelial repair. Stent, lumen and neointimal areas were measured from histological sections obtained from eight right coronary stented porcine arter

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Pei, Hong, Jiali Gu, Pushpa-Rekha Thimmalapura, Angeles Mison, and Jerry L. Nadler. "Activation of the 12-lipoxygenase and signal transducer and activator of transcription pathway during neointima formation in a model of the metabolic syndrome." American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (2006): E92—E102. http://dx.doi.org/10.1152/ajpendo.00133.2005.

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Insulin resistance (IR) is associated with an increased risk of cardiovascular diseases. The obese Zucker rat (ZR) is a model of IR that shows markedly increased insulin and triglyceride concentrations without major changes in glucose. In this study, we evaluated the response of obese and lean ZR to carotid balloon injury and determined potential mechanisms and treatments. The neointima-to-media ratio of obese ZR was greater than that of lean ZR, starting at 14 days after injury, and persisted until at least day 30. An enhanced inflammatory response to balloon injury in the obese ZR was reflec

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Guo, June, Troy J. Pereira, Yusaku Mori, et al. "Resveratrol Inhibits Neointimal Growth after Arterial Injury in High-Fat-Fed Rodents: The Roles of SIRT1 and AMPK." Journal of Vascular Research 57, no. 6 (2020): 325–40. http://dx.doi.org/10.1159/000509217.

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We have shown that both insulin and resveratrol (RSV) decrease neointimal hyperplasia in chow-fed rodents via mechanisms that are in part overlapping and involve the activation of endothelial nitric oxide synthase (eNOS). However, this vasculoprotective effect of insulin is abolished in high-fat-fed insulin-resistant rats. Since RSV, in addition to increasing insulin sensitivity, can activate eNOS via pathways that are independent of insulin signaling, such as the activation of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), we speculated that unlike insulin, the vasculoprotective effect of

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Erami, Cauveh, Hua Zhang, Jason G. Ho, David M. French та James E. Faber. "α1-Adrenoceptor stimulation directly induces growth of vascular wall in vivo". American Journal of Physiology-Heart and Circulatory Physiology 283, № 4 (2002): H1577—H1587. http://dx.doi.org/10.1152/ajpheart.00218.2002.

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Previous studies suggesting that norepinephrine is directly trophic for the vascular wall have been confounded by concomitant hemodynamic disturbances. Herein, a microcatheter connected to an osmotic minipump was implanted adjacent to the rat carotid for 2-wk perivascular suffusion of agents at systemic levels ∼1,000 times below the threshold for altering arterial pressure. Norepinephrine decreased lumen and adventitial areas and circumference by 10, 14, and 5%, respectively (all P < 0.05); a nonsubtype-specific α1-adrenoceptor (AR) antagonist had no effect. When begun at the time of balloo

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Teeters, John C., Cauveh Erami, Hua Zhang та James E. Faber. "Systemic α1A-adrenoceptor antagonist inhibits neointimal growth after balloon injury of rat carotid artery". American Journal of Physiology-Heart and Circulatory Physiology 284, № 1 (2003): H385—H392. http://dx.doi.org/10.1152/ajpheart.00658.2002.

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Previous in vitro and in vivo studies have shown that norepinephrine, acting through α1A-adrenoceptors, stimulates hypertrophy, proliferation, and migration of vascular smooth muscle cells and adventitial fibroblasts and may contribute to neointimal growth, lumen loss, and inward remodeling caused by iatrogenic wall injury and vascular disease. Our present aim was to determine whether intravenous administration of the α1A-adrenoceptor antagonist KMD-3213, at dosages without systemic hemodynamic effects, inhibits wall growth after injury. Inhibition of α1A-adrenoceptors with 12.8 and 32 μg/kg K

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Yang, Feng, Qishan Chen, Mei Yang, et al. "Macrophage-derived MMP-8 determines smooth muscle cell differentiation from adventitia stem/progenitor cells and promotes neointima hyperplasia." Cardiovascular Research 116, no. 1 (2019): 211–25. http://dx.doi.org/10.1093/cvr/cvz044.

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Abstract Aims Emerging evidence has suggested that adventitia stem/progenitor cells (AdSPCs) migrate into the intima of arteries in response to injury, where they differentiate towards smooth muscle cells (SMCs) and participate in neointimal hyperplasia. We have previously identified matrix metalloproteinase-8 (MMP8) as a key player in atherogenesis. In this study, we aimed to investigate the functional roles of macrophage-derived MMP8 in AdSPC differentiation and injury-induced arterial remodelling. Methods and results We first observed an important role for MMP8 in SMC differentiation from e

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Yang, Jun, Jian Luo, Deng Biao, Shu Yan Wang, Sai Liang Ding та Zhi Xiong Wu. "Saporin Conjugated with Transforming Growth Factor-α Inhibit Neointimal Proliferation by Specific Cytotoxicity". Advanced Materials Research 904 (березень 2014): 249–52. http://dx.doi.org/10.4028/www.scientific.net/amr.904.249.

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Objective This study aimed to investigate the Cytotoxic effects of TGFα-SAP on the inhibition of neointimal proliferation after rat common carotid arterial injury. Methods seventy rats were divided into two groups. The TGFα-SAP treated group was treated with local injection of TGFα-SAP (5μg/kg) after injury, and the control group was treated with saline. Rat arterial segment was investigated at 1, 3, 9, and 28 days after operation. Results Compared to the control group, the TGFα-SAP treated group shows a significant inhibition of intimal thickness. Conclusion The results indicated that TGFα-SA

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Guo, Ling, Wenhu Ning, Zhen Tan, Zhaowei Gong, and Xueqi Li. "Mechanism of matrix metalloproteinase axis-induced neointimal growth." Journal of Molecular and Cellular Cardiology 66 (January 2014): 116–25. http://dx.doi.org/10.1016/j.yjmcc.2013.11.014.

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Parmentier, Jean-Hugues, Chunxiang Zhang, Anne Estes, Susan Schaefer та Kafait U. Malik. "Essential role of PKC-ζ in normal and angiotensin II-accelerated neointimal growth after vascular injury". American Journal of Physiology-Heart and Circulatory Physiology 291, № 4 (2006): H1602—H1613. http://dx.doi.org/10.1152/ajpheart.01363.2005.

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The contribution of atypical protein kinase C (PKC)-ζ to ANG II-accelerated restenosis after endoluminal vascular injury was investigated by using the rat carotid balloon injury model. Exposure of injured arteries to ANG II resulted in an extensive neointimal thickening (1.9 times) compared with vehicle at day 14. Treatment with PKC-ζ antisense, but not scrambled, oligonucleotides reduced neointimal formation observed in the presence or absence of ANG II. Examination of early events (2 days) after injury showed an increase in cellularity in the perivascular area of the artery wall that was tra

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Ni, Zhichao, Jiacheng Deng, Claire M. F. Potter, et al. "Recipient c-Kit Lineage Cells Repopulate Smooth Muscle Cells of Transplant Arteriosclerosis in Mouse Models." Circulation Research 125, no. 2 (2019): 223–41. http://dx.doi.org/10.1161/circresaha.119.314855.

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Rationale: Transplantation-accelerated arteriosclerosis is one of the major challenges for long-term survival of patients with solid organ transplantation. Although stem/progenitor cells have been implicated to participate in this process, the cells of origin and underlying mechanisms have not been fully defined. Objective: The objective of our study was to investigate the role of c-Kit lineage cells in allograft-induced neointima formation and to explore the mechanisms underlying this process. Methods and Results: Using an inducible lineage tracing Kit-CreER;Rosa26-tdTomato mouse model, we ob

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Mei, Xiaohan, Xiao-Bing Cui, Yiran Li, and Shi-You Chen. "CircSOD2: A Novel Regulator for Smooth Muscle Proliferation and Neointima Formation." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 12 (2021): 2961–73. http://dx.doi.org/10.1161/atvbaha.121.316911.

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Objective: Vascular smooth muscle cell (SMC) proliferation contributes to neointima formation following vascular injury. Circular RNA—a novel type of noncoding RNA with closed-loop structure—exhibits cell- and tissue-specific expression patterns. However, the role of circular RNA in SMC proliferation and neointima formation is largely unknown. The objective of this study is to investigate the role and mechanism of circSOD2 in SMC proliferation and neointima formation. Approach and Results: Circular RNA profiling of human aortic SMCs revealed that PDGF (platelet-derived growth factor)-BB up- an

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HU, Cheng-heng, Xiao KE, Kui CHEN, Da-ya YANG, Zhi-min DU, and Gui-fu WU. "Transplantation of human umbilical cord-derived endothelial progenitor cells promotes re-endothelialization of the injured carotid artery after balloon injury in New Zealand white rabbits." Chinese Medical Journal 126, no. 8 (2013): 1480–85. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20122355.

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Background Cell transplantation has great potential for promoting endothelial repair and reducing the complications of percutaneous coronary intervention (PCI). The aim of this study was to investigate the effect of transplantation of human umbilical cord blood endothelial progenitor cells (EPCs) on injured arteries. Methods Umbilical cord blood mononuclear cells were obtained from post-partum lying-in women, and EPCs were isolated, cultured, expanded and identified by immunofluorescence. The carotid arterial endothelium of New Zealand white rabbits was injured by dilatation with a 3F balloon,

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Liu, S. Q., L. Zhong, and J. Goldman. "Control of the Shape of a Thrombus-Neointima-Like Structure by Blood Shear Stress." Journal of Biomechanical Engineering 124, no. 1 (2001): 30–36. http://dx.doi.org/10.1115/1.1428744.

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Fluid mechanical factors are thought to influence vascular morphogenesis. Here we show how blood shear stress regulates the shape of a thrombus-neointima-like tissue on a polymer micro-cylinder implanted in the center of the rat vena cava with the micro-cylinder perpendicular to blood flow. In this model, the micro-cylinder is exposed to a laminar flow with a known shear stress field in the leading region and a vortex flow in the trailing region. At 1, 5, 10, 20, and 30 days after implantation, it was found that the micro-cylinder was encapsulated by a thrombus-neointima-like tissue with a str

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Yamamoto, Kei, Ryuichi Morishita, Naruya Tomita та ін. "Novel Therapeutic Strategy for Restenosis Using Ribozyme Oligonucleotides Against Transforming Growth Factor-β". Hypertension 36, suppl_1 (2000): 728–29. http://dx.doi.org/10.1161/hyp.36.suppl_1.728-e.

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P197 Background Since the mechanisms of atherosclerosis or restenosis after angioplasty have been postulated to involve an increase in TGF-β, a selective decrease in TGF-βmay have therapeutic value. Thus, we employed the ribozyme a unique class of RNA molecules that not only store information but also process catalytic activity, to selectively inhibit TGF-βexpression. Methods & Results We constructed ribozyme oligonucleotides targeted to the sequence of TGF-βgene which shows 100 % homology among human, rat and mouse. The specificity of ribozyme against TGF-βgene was confirmed by selective

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Kohno, Takashi, Norifumi Urao, Takashi Ashino та ін. "IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury". American Journal of Physiology-Cell Physiology 305, № 6 (2013): C591—C600. http://dx.doi.org/10.1152/ajpcell.00011.2013.

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Platelet-derived growth factor (PDGF) stimulates vascular smooth muscle cell (VSMC) migration and neointimal formation in response to injury. We previously identified IQ-domain GTPase-activating protein 1 (IQGAP1) as a novel VEGF receptor 2 binding scaffold protein involved in endothelial migration. However, its role in VSMC migration and neointimal formation in vivo is unknown. Here we show that PDGF stimulation rapidly promotes IQGAP1 association with PDGF receptor-β (PDGFR) as well as IQGAP1 tyrosine phosphorylation in cultured VSMC. Overexpression or knockdown of IQGAP1 enhances or inhibit

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Cohen-Sela, Einat, David Dangoor, Hila Epstein, et al. "Nanospheres of a Bisphosphonate Attenuate Intimal Hyperplasia." Journal of Nanoscience and Nanotechnology 6, no. 9 (2006): 3226–34. http://dx.doi.org/10.1166/jnn.2006.428.

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The present study explored a novel strategy for attenuation of restenosis after arterial injury by a bisphosphonate encapsulated in polymeric nanoparticles (NP) for transient selective depletion of macrophages. A bisphosphonate (BP), 2-(2-Aminopyrimidino) ethyldiene-1,1-bisphosphonic acid betaine (ISA), was successfully formulated in 400 nm sized polylactide/glycolide-based NP with high yield (69%) and entrapment efficiency (60% w/w). ISA NP, but not blank NP or free ISA, exhibited specific and significant cytotoxic effect on macrophages-like RAW 264 cells, in a dose-dependent manner, with no

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Watt, Jonathan, Roger Wadsworth, Simon Kennedy, and Keith G. Oldroyd. "Pro-healing drug-eluting stents: a role for antioxidants?" Clinical Science 114, no. 4 (2008): 265–73. http://dx.doi.org/10.1042/cs20070207.

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Current strategies to lower the incidence of ISR (in-stent restenosis) following PCI (percutaneous coronary intervention) are aimed at modifying arterial healing after stent injury. This can impair endothelial recovery and render the vessel prone to acute thrombosis. As early restoration of endothelial integrity inhibits neointimal growth and thrombosis, alternative approaches which encourage this process may provide a more effective long-term result after PCI. Oxidative stress is enhanced after PCI and participates in the regulation of endothelial regeneration and neointimal growth. Moreover,

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Kuznetsov, Konstantin A., Ivan S. Murashov, Vera S. Chernonosova, et al. "Vascular Stents Coated with Electrospun Drug-Eluting Material: Functioning in Rabbit Iliac Artery." Polymers 12, no. 8 (2020): 1741. http://dx.doi.org/10.3390/polym12081741.

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A stenting procedure aimed at blood flow restoration in stenosed arteries significantly improves the efficiency of vascular surgery. However, the current challenge is to prevent neointimal growth, which reduces the vessel lumen, in the stented segments in the long run. We tested in vivo drug-eluting coating applied by electrospinning to metal vascular stents to inhibit the overgrowth of neointimal cells via both the drug release and mechanical support of the vascular wall. The blend of polycaprolactone with human serum albumin and paclitaxel was used for stent coating by electrospinning. The d

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Diaz-Rodriguez, Sergio, Charlotte Rasser, Jules Mesnier, et al. "Coronary stent CD31-mimetic coating favours endothelialization and reduces local inflammation and neointimal development in vivo." European Heart Journal 42, no. 18 (2021): 1760–69. http://dx.doi.org/10.1093/eurheartj/ehab027.

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Abstract Aims The rapid endothelialization of bare metal stents (BMS) is counterbalanced by inflammation-induced neointimal growth. Drug-eluting stents (DES) prevent leukocyte activation but impair endothelialization, delaying effective device integration into arterial walls. Previously, we have shown that engaging the vascular CD31 co-receptor is crucial for endothelial and leukocyte homeostasis and arterial healing. Furthermore, we have shown that a soluble synthetic peptide (known as P8RI) acts like a CD31 agonist. The aim of this study was to evaluate the effect of CD31-mimetic metal stent

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Kataoka, Toru, Eberhard Grube, Yasuhiro Honda, et al. "7-Hexanoyltaxol–Eluting Stent for Prevention of Neointimal Growth." Circulation 106, no. 14 (2002): 1788–93. http://dx.doi.org/10.1161/01.cir.0000031734.11420.1c.

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Schäfer, Katrin, Martin Halle, Colin Goeschen, et al. "Leptin Promotes Vascular Remodeling and Neointimal Growth in Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 24, no. 1 (2004): 112–17. http://dx.doi.org/10.1161/01.atv.0000105904.02142.e7.

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Reidy, Michael A., Christopher Jackson, and Volkhard Lindner. "Neointimal Proliferation: Control of Vascular Smooth Muscle Cell Growth." Vascular Medicine Review vmr-3, no. 2 (1992): 156–67. http://dx.doi.org/10.1177/1358863x9200300206.

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Tahir, Hannan, Ioana Niculescu, Carles Bona-Casas, Roeland M. H. Merks, and Alfons G. Hoekstra. "An in silico study on the role of smooth muscle cell migration in neointimal formation after coronary stenting." Journal of The Royal Society Interface 12, no. 108 (2015): 20150358. http://dx.doi.org/10.1098/rsif.2015.0358.

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Excessive migration and proliferation of smooth muscle cells (SMCs) has been observed as a major factor contributing to the development of in-stent restenosis after coronary stenting. Building upon the results from in vivo experiments, we formulated a hypothesis that the speed of the initial tissue re-growth response is determined by the early migration of SMCs from the injured intima. To test this hypothesis, a cellular Potts model of the stented artery is developed where stent struts were deployed at different depths into the tissue. An extreme scenario with a ruptured internal elastic lamin

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Cui, Song, Jing-Hua Liu, Xian-Tao Song, et al. "A Novel Stent Coated with Antibodies to Endoglin Inhibits Neointimal Formation of Porcine Coronary Arteries." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/428619.

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Endoglin/CD105 is an accessory protein of the transforming growth factor-βreceptor system that plays a critical role in proliferation of endothelial cells and neovasculature. Here, we aimed to assess the effect of novel stents coated with antibodies to endoglin (ENDs) on coronary neointima formation. Thirty ENDs, thirty sirolimus-eluting stents (SESs), and thirty bare metal stents (BMSs) were randomly assigned and placed in the coronary arteries in 30 juvenile pigs. Histomorphometric analysis and scanning electron microscopy were performed after stent implantation. Our results showed that afte

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Mnjoyan, Zakar H., Dennis Doan, Jimi Lynn Brandon, et al. "The critical role of the intrinsic VSMC proliferation and death programs in injury-induced neointimal hyperplasia." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (2008): H2276—H2284. http://dx.doi.org/10.1152/ajpheart.91527.2007.

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Postangioplasty and in-stent restenosis remain ominous problems in percutaneous coronary intervention where good animal models of restenosis proneness and resistance are needed. We accidentally discovered that the carotid arteries (CAs) of the Harlan and Sasco substrains of Sprague-Dawley rats display drastically different restenosis phenotypes following balloon-induced endothelial denudation. When subjected to balloon injury, Sasco CAs exhibited significantly larger neointimal mass than did Harlan CAs at both days 14 and 32, as evidenced by a higher intima-to-media ratio and a greater number

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Christie, D. Benjamin, Jing Kang, Dennis W. Ashley, et al. "Accelerated Migration and Proliferation of Smooth Muscle Cells Cultured from Neointima Induced by a Vena Cava Filter." American Surgeon 72, no. 6 (2006): 491–96. http://dx.doi.org/10.1177/000313480607200606.

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Formation of a neointima is associated with grafted artery or vein, angioplasty, and stent and inferior vena cava filter (IVCF) implantation. Contributing to the neointima is a population of vascular smooth muscle cells (SMC) that migrates from media and subsequently proliferates within intima. The purpose of this present study was to culture SMC from normal vessel wall and from neointima and to compare migration and growth of these cells. Neointima was stimulated in the vena cava of pigs by placement of an IVCF for 30 days. Tissue was taken from the thickened wall between the struts and from

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van Albada, Mirjam E., Beatrijs Bartelds, Hans Wijnberg, et al. "Gene expression profile in flow-associated pulmonary arterial hypertension with neointimal lesions." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 4 (2010): L483—L491. http://dx.doi.org/10.1152/ajplung.00106.2009.

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Pulmonary arterial hypertension (PAH) is a pulmonary angioproliferative disease with high morbidity and mortality, characterized by a typical pattern of pulmonary vascular remodeling including neointimal lesions. In congenital heart disease, increased pulmonary blood flow has appeared to be a key mediator in the development of these characteristic lesions, but the molecular mechanisms underlying the pulmonary vascular lesions are largely unknown. We employed a rat model of flow-associated PAH, which induced specific pulmonary neointimal lesions. We identified gene expression profiles in rats s

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Chiang, Simon, Danna M. Breen, June Guo, Yusaku Mori, and Adria Giacca. "Local insulin application on the carotid artery inhibits neointima formation." Canadian Journal of Physiology and Pharmacology 91, no. 12 (2013): 1086–94. http://dx.doi.org/10.1139/cjpp-2013-0038.

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Anti-mitogenic agents currently used to prevent restenosis in drug-eluting stents delay re-endothelialization. Delayed re-endothelialization is now considered as the main cause of late stent thrombosis with drug-eluting stents, which emphasizes the need for new treatments. We have shown that systemic insulin treatment decreases neointimal growth and accelerates re-endothelialization after arterial injury in a rat model of restenosis. However, systemic insulin treatment cannot be given to non-diabetic individuals because of the risk of hypoglycemia. Thus, we investigated whether local insulin t

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