scholarly journals Impact of the Consumption of Tea Polyphenols on Early Atherosclerotic Lesion Formation and Intestinal Bifidobacteria in High-Fat-Fed ApoE−/− Mice

2016 ◽  
Vol 3 ◽  
Author(s):  
Zhen-Lin Liao ◽  
Ben-Hua Zeng ◽  
Wei Wang ◽  
Gui-Hua Li ◽  
Fei Wu ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Tea Polyphenols ◽  
High Fat ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Atherosclerotic Lesion Formation

Abstract 83: Bone Marrow Derived Cells Do Not Mediate Reductions in Cholesterol, Atherosclerosis and Adiposity in Microsomal Prostaglindin E Synthase 1 Deficient Mice Fed High Fat Diets Enriched in Cholesterol

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Bone Marrow ◽  
Weight Gain ◽  
Marrow Cell ◽  
Atherosclerotic Lesion ◽  
Chimeric Mice ◽  
High Fat ◽  
Lesion Formation ◽  
Bone Marrow Derived Cells ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Microsomal prostaglandin E 2 synthase-1 (mPGES-1) catalyzes the conversion of COX-2 generated PGH 2 to PGE 2 and is the predominate source of PGE 2 during and inflammatory response. We and others have demonstrated that mPGES-1 deficiency attenuates atherosclerosis in mice on a mixed background. The present study investigated the effect of mPGES-1 deficiency on atherosclerosis in C57BL/6 low density lipoprotein receptor deficient (LDLr-/-) mice. mPGES-1 deficiency attenuated atherosclerosis in LDLr-/- mice fed either a low fat (LF) (P = 0.02) or high fat (HF) (P = 0.0026) diet enriched with cholesterol, or a western diet (P = 0.02) for 17 weeks. mPGES-1 deficiency attenuated weight gain and cholesterol concentrations in mice fed a western (P = 0.004 and P < 0.05; respectively) or HF diet (P = 0.01 and P = 0.012, respectively). However, body weight and cholesterol concentrations were not different in mice fed the LF diet. These data suggest that different mechanisms mediate the reduction in atherosclerosis in mPGES-1 deficient mice fed LF and HF diets. To determine if mPGES-1 deficiency in macrophages contributed to the reduction in atherosclerosis in mice fed HF diets, 4 groups of chimeric mice were generated. Four weeks post bone marrow cell transplant (BMT) mice were fed a western diet. BMT attenuated weight gain in all groups of chimeric mice; however, weight gain was not different between any of the groups. BMT decreased atherosclerotic lesion formation 10 fold in all groups of mice. Neither bone marrow cell specific deficiency of mPGES-1 (KO>WT) or mPGES-1 specific expression in bone marrow derived cells (WT>KO) had an effect on lesion formation compared to WT>WT or KO>KO mice. Cholesterol concentrations were decreased in KO>KO and WT>KO mice compared to WT>WT (P < 0.01) and KO>WT (P< 0.05) mice. These data suggest that mPGES-1 expression in bone marrow derived cells does not contribute to the development of atherosclerosis. Moreover, these data suggest that prostanoids may play a role in hepatic cholesterol homeostasis in mice fed HF diets enriched in cholesterol thereby contributing to atherosclerotic lesion formation. Moreover, these data provide further evidence that prostanoids play a role in regulating the accumulation of diet-induced adiposity.

scholarly journals Aldose Reductase Protects Against Early Atherosclerotic Lesion Formation in Apolipoprotein E-Null Mice

2009 ◽  
Vol 105 (8) ◽  
pp. 793-802 ◽  
Author(s):  
Sanjay Srivastava ◽  
Elena Vladykovskaya ◽  
Oleg A. Barski ◽  
Matthew Spite ◽  
Karin Kaiserova ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Aldose Reductase ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Atherosclerotic Lesion Formation

scholarly journals Cyclooxygenase-2 Promotes Early Atherosclerotic Lesion Formation in LDL Receptor–Deficient Mice

Circulation ◽  
2002 ◽  
Vol 105 (15) ◽  
pp. 1816-1823 ◽  
Author(s):  
Michael E. Burleigh ◽  
Vladimir R. Babaev ◽  
John A. Oates ◽  
Raymond C. Harris ◽  
Shiva Gautam ◽  
...  
Keyword(s):  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Cyclooxygenase 2 ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

scholarly journals Rho-Associated Protein Kinase Contributes to Early Atherosclerotic Lesion Formation in Mice

2003 ◽  
Vol 93 (9) ◽  
pp. 884-888 ◽  
Author(s):  
Ziad Mallat ◽  
Andrea Gojova ◽  
Vincent Sauzeau ◽  
Valérie Brun ◽  
Jean-Sébastien Silvestre ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Atherosclerotic Lesion Formation

Abstract 13248: DPP-4 Inhibition Reduces Atherosclerosis by Priming Monocytes into Alternative M2 Macrophages

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Christoph Brenner ◽  
Wolfgang M Franz ◽  
Sarah Kuehlenthal ◽  
Kira Kuschnerus ◽  
Friederike Remm ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Macrophage Polarization ◽  
Atherosclerotic Lesion ◽  
Plaque Burden ◽  
Western World ◽  
M2 Macrophages ◽  
High Fat ◽  
Lesion Formation ◽  
Therapeutic Concept ◽  
Atherosclerotic Lesion Formation

Introduction: Major parts of the population in the western world are suffering from atherosclerotic diseases like coronary and peripheral artery disease or stroke. Interventional and pharmacological therapies at present focus on the treatment of vascular stenoses, secondary prophylaxis or reduction of cardiovascular risk factors. Hypothesis: In this project, we want to establish the pharmacological inhibition of DPP4 as a new therapeutic concept focussing on macrophage polarization during development of atherosclerosis. Methods: Non-diabetic ApoE-/- mice were treated with normal diet or high fat diet for three months to induce arterial atherosclerotic lesion formation. The descending aorta was stained using Oil-Red-O to quantify atherosclerotic lesions. In parallel mice were treated with Sitagliptin or placebo. Macrophage subtype content (M1, M2) in the aortic wall was quantified using FACS. Results: Mice on high fat diet treated with Sitagliptin showed a dramatic reduction in atherosclerotic lesion formation in contrast to placebo treated animals. Regarding total macrophage content in the vascular wall we could not detect a difference between the treatment groups. However, the number of protective M2 macrophages was more than tripled in the gliptin-treated animals. Moreover, the number of mural M2 macrophages inversely correlated with the aortic plaque burden. In further analyses we could demonstrate that Sitagliptin favoured macrophage polarization to alternatively activated M2 macrophages via the CXCR4-signaling pathway. Conclusions: We demonstrated that long-term Sitagliptin treatment in ApoE-/- animals on high fat diet can successfully inhibit atherosclerotic lesion formation via induction of macrophage polarization to the protective M2 phenotype. Due to the promising results of this study we are currently planning to transfer the underlying therapeutical concept into a randomized clinical trial.

scholarly journals Hematopoietic Deficiency of the Long Noncoding RNA MALAT1 Promotes Atherosclerosis and Plaque Inflammation

Circulation ◽  
2019 ◽  
Vol 139 (10) ◽  
pp. 1320-1334 ◽  
Author(s):  
Sebastian Cremer ◽  
Katharina M. Michalik ◽  
Ariane Fischer ◽  
Larissa Pfisterer ◽  
Nicolas Jaé ◽  
...  
Keyword(s):  
Bone Marrow ◽  
High Fat Diet ◽  
Bone Marrow Cells ◽  
Hematopoietic Cells ◽  
Atherosclerotic Lesion ◽  
High Fat ◽  
Lesion Formation ◽  
Control Of Gene Expression ◽  
Atherosclerotic Lesion Formation ◽  
Marrow Cells

Background:The majority of the human genome comprises noncoding sequences, which are in part transcribed as long noncoding RNAs (lncRNAs). lncRNAs exhibit multiple functions, including the epigenetic control of gene expression. In this study, the effect of the lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) on atherosclerosis was examined.Methods:The effect of MALAT1 on atherosclerosis was determined in apolipoprotein E–deficient (Apoe−/−) MALAT1-deficient (Malat1−/−) mice that were fed with a high-fat diet and by studying the regulation of MALAT1 in human plaques.Results:Apoe−/−Malat1−/−mice that were fed a high-fat diet showed increased plaque size and infiltration of inflammatory CD45+cells compared with Apoe−/−Malat1+/+control mice. Bone marrow transplantation of Apoe−/−Malat1−/−bone marrow cells in Apoe−/−Malat1+/+mice enhanced atherosclerotic lesion formation, which suggests that hematopoietic cells mediate the proatherosclerotic phenotype. Indeed, bone marrow cells isolated from Malat1−/−mice showed increased adhesion to endothelial cells and elevated levels of proinflammatory mediators. Moreover, myeloid cells of Malat1−/−mice displayed enhanced adhesion to atherosclerotic arteries in vivo. The anti-inflammatory effects of MALAT1 were attributed in part to reduction of the microRNA miR-503. MALAT1 expression was further significantly decreased in human plaques compared with normal arteries and was lower in symptomatic versus asymptomatic patients. Lower levels of MALAT1 in human plaques were associated with a worse prognosis.Conclusions:Reduced levels of MALAT1 augment atherosclerotic lesion formation in mice and are associated with human atherosclerotic disease. The proatherosclerotic effects observed in Malat1−/−mice were mainly caused by enhanced accumulation of hematopoietic cells.

Role of fibrinopeptide B in early atherosclerotic lesion formation

1990 ◽  
Vol 160 (2) ◽  
pp. 156-159 ◽  
Author(s):  
Tej M. Singh ◽  
Mark H. Kadowaki ◽  
Seymour Glagov ◽  
Christopher K. Zarins
Keyword(s):  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Atherosclerotic Lesion Formation

scholarly journals Dietary Carnosine Prevents Early Atherosclerotic Lesion Formation in Apolipoprotein E–Null Mice

2013 ◽  
Vol 33 (6) ◽  
pp. 1162-1170 ◽  
Author(s):  
Oleg A. Barski ◽  
Zhengzhi Xie ◽  
Shahid P. Baba ◽  
Srinivas D. Sithu ◽  
Abhinav Agarwal ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Early Atherosclerotic Lesion ◽  
Atherosclerotic Lesion Formation

Pneumococcal vaccination decreases atherosclerotic lesion formation: molecular mimicry between Streptococcus pneumoniae and oxidized LDL

10.1038/nm876 ◽  
2003 ◽  
Vol 9 (6) ◽  
pp. 736-743 ◽  
Author(s):  
Christoph J Binder ◽  
Sohvi Hörkkö ◽  
Asheesh Dewan ◽  
Mi-Kyung Chang ◽  
Emily P Kieu ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Molecular Mimicry ◽  
Oxidized Ldl ◽  
Pneumococcal Vaccination ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Atherosclerotic Lesion Formation
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