scholarly journals Crucial Role of the CCL2/CCR2 Axis in Neointimal Hyperplasia After Arterial Injury in Hyperlipidemic Mice Involves Early Monocyte Recruitment and CCL2 Presentation on Platelets

2004 ◽  
Vol 95 (11) ◽  
pp. 1125-1133 ◽  
Author(s):  
Andreas Schober ◽  
Alma Zernecke ◽  
Elisa A. Liehn ◽  
Philipp von Hundelshausen ◽  
Sandra Knarren ◽  
...  
2020 ◽  
Vol 57 (6) ◽  
pp. 325-340
Author(s):  
June Guo ◽  
Troy J. Pereira ◽  
Yusaku Mori ◽  
Marel Gonzalez Medina ◽  
Danna M. Breen ◽  
...  

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 RSV would be retained in high-fat-fed rats. We found that high-fat feeding decreased insulin sensitivity and increased neointimal area and that RSV improved insulin sensitivity (<i>p &#x3c;</i> 0.05) and decreased neointimal area in high-fat-fed rats (<i>p &#x3c;</i> 0.05). We investigated the role of SIRT1 in the effect of RSV using two genetic mouse models. We found that RSV decreased neointimal area in high-fat-fed wild-type mice (<i>p &#x3c;</i> 0.05), an effect that was retained in mice with catalytically inactive SIRT1 (<i>p &#x3c;</i> 0.05) and in heterozygous SIRT1-null mice. In contrast, the effect of RSV was abolished in AMKPα2-null mice. Thus, RSV decreased neointimal hyperplasia after arterial injury in both high-fat-fed rats and mice, an effect likely not mediated by SIRT1 but by AMPKα2.


Blood ◽  
2006 ◽  
Vol 107 (11) ◽  
pp. 4240-4243 ◽  
Author(s):  
Alma Zernecke ◽  
Elisa A. Liehn ◽  
Ji-Liang Gao ◽  
William A. Kuziel ◽  
Philip M. Murphy ◽  
...  

AbstractThe chemokine RANTES has been implicated in neointimal hyperplasia after arterial injury. We analyzed the differential role of the RANTES receptors CCR1 and CCR5 by genetic deletion in apolipoprotein E–deficient mice. Deficiency in CCR5 significantly reduced neointimal area after arterial wire injury, associated with a decrease in macrophages, CD3+ T lymphocytes, and CCR2+ cells. In contrast, CCR1 deficiency did not affect neointimal area or cell content. Deletion of CCR5 entailed an up-regulation of the anti-inflammatory cytokine interleukin 10 (IL-10) in neointimal smooth muscle cells, and its antibody blockade reversed effects in CCR5–/– mice. Conversely, proinflammatory interferon γ was increased in the neointima of CCR1–/– mice, and its blockade unmasked a reduction in macrophage recruitment. Our data indicate that CCR5 is more crucial than CCR1 for neointimal plaque formation, and that its attenuation in CCR5–/– mice is due to an atheroprotective immune response involving IL-10. This harbors important implications for targeting chemokine receptors in vascular remodeling.


2020 ◽  
Vol 9 (5) ◽  
Author(s):  
Edmund B. Chen ◽  
Katherine E. Shapiro ◽  
Kelly Wun ◽  
Thomas Kuntz ◽  
Betty R. Theriault ◽  
...  

Background The potential role of the gut microbiome in cardiovascular diseases is increasingly evident. Arterial restenosis attributable to neointimal hyperplasia after cardiovascular procedures such as balloon angioplasty, stenting, and bypass surgery is a common cause of treatment failure, yet whether gut microbiota participate in the development of neointimal hyperplasia remains largely unknown. Methods and Results We performed fecal microbial transplantation from conventionally raised male C57BL/6 mice to age‐, sex‐, and strain‐matched germ‐free mice. Five weeks after inoculation, all mice underwent unilateral carotid ligation. Neointimal hyperplasia development was quantified after 4 weeks. Conventionally raised and germ‐free cohorts served as comparison groups. Conclusions Germ‐free mice have significantly attenuated neointimal hyperplasia development compared with conventionally raised mice. The arterial remodeling response is restored by fecal transplantation. Our results describe a causative role of gut microbiota in contributing to the pathogenesis of neointimal hyperplasia.


2001 ◽  
Vol 11 (PR11) ◽  
pp. Pr11-47-Pr11-52
Author(s):  
V. M. Pan ◽  
V. S. Flis ◽  
V. A. Komashko ◽  
O. G. Plys ◽  
C. G. Tretiatchenko ◽  
...  

1997 ◽  
Vol 77 (04) ◽  
pp. 783-788 ◽  
Author(s):  
Paolo Golino ◽  
Giuseppe Ambrosio ◽  
Massimo Ragni ◽  
Plinio Cirillo ◽  
Nicolino Esposito ◽  
...  

SummaryRestenosis following coronary angioplasty is thought to result from migration and proliferation of medial smooth muscle cells. However, the factors that initiate this proliferation are still unknown. In a rabbit model of carotid artery injury, we tested the hypothesis that activated platelets and leucocytes might contribute to the development of neointimal hyperplasia. Following arterial injury, rabbits received either no treatment, R15.7, a monoclonal antibody against the leucocyte CD ll/CD 18 adhesion complex, aurintricarboxylic acid (ATA), a sub stance that inhibits platelet glycoprotein Ib-von Willebrand factor interaction, or the combination of R15.7 and ATA. After 21 days, the extent of neointimal hyperplasia was evaluated by planimetry on histological arterial sections. The area of neointima averaged 0.51 ±0.07 mm2 in control animals and it was significantly reduced by administrationof either R15.7 or ATA alone to 0.12 ± 0.05 and 0.20 ±0.01 mm2, respectively (p <0.05 vs controls for both groups). The animals that received the combination of R15.7 and ATA showed a further reduction in neointimal hyperplasia, as compared to animals that received ATA alone (p <0.05 vs ATA alone). These data indicate that platelets and leucocytes play animportant role in the pathophysi ology of neointimal hyperplasia in this experimental model. Interven tions that reduce platelet and leucocyte adhesion to vessel wall might have beneficial effects in reducing restenosis following coronary angioplasty.


Jurnal Akta ◽  
2017 ◽  
Vol 4 (3) ◽  
pp. 463
Author(s):  
Muslim Ansori ◽  
Akhmad Khisni

With the enactment of the Education System Act no 20 of 2003 (better known as the Sisdiknas Act), the State has determined that educational institutions should have a legal umbrella in the form of a legal entity, or better known as the Legal Entity Education. As a non-profit organization, the Foundation is the right legal entity that becomes a place for educational institutions, especially private schools. Therefore, of course, Notary has a very crucial role in making notary deed in the form of establishment and deed of change, such as example how in making the right basic budget and not multi interpresatasi for stake holders in the foundation. Therefore, the role of function and authority of the organ of the foundation must be clearly stated in the articles of association, so as not to cause a dispute in the future.KEYWORDS: Notaries, Foundation, Organ Foundation,


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