Expansive Growth of Atherosclerotic Plaques Assessed by VH-IVUS - Association with TNF-α and OX-LDL Levels in Circulation

2013 ◽  
Keyword(s):  
Atherosclerotic Plaques ◽  
Tnf Α

scholarly journals Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque responses

2019 ◽  
Author(s):  
S Oggero ◽  
M de Gaetano ◽  
S Marcone ◽  
M Barry ◽  
T Montero-Melendez ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Platelet Activation ◽  
Vascular Inflammation ◽  
Atherosclerotic Plaques ◽  
Disease Development ◽  
Tnf Α ◽  
Mixed Aggregates ◽  
Key Players ◽  
Platelet Aggregates ◽  
Progression Of Atherosclerosis

AbstractIn atherosclerosis, a chronic disease characterized by lipid accumulation, fibrosis and vascular inflammation, extracellular vesicles (EVs) are emerging as key players in different stages of disease development. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF-α are both CD14+ and CD41+. Tempering platelet activation with Iloprost™ impacted the quality and quantity of EV produced. Proteomics of EVs from cells activated with TNF-α alone or in presence Iloprost™ revealed distinct proteome, with selective hits like gelsolin. EVs from TNF-α stimulated monocytes augmented release of cytokines, and modulated more than 500 proteins by proteomics, when added to human atherosclerotic plaques. In contrast, EVs generated by TNF-α and Iloprost™ produced minimal plaque activation. In conclusion, attenuating platelet activation has an effect on EV composition released from monocyte/platelet aggregates with downstream modulation of their pro-inflammatory actions and contribution to the development and progression of atherosclerosis.

scholarly journals The relationship of serum leptin, serum TNF-α, plasma lipids and obesity parameters in patients treated with weight neutral antidepressants

2018 ◽  
Vol 6 (2) ◽  
pp. 465
Author(s):  
Naveen Kumar Reddy Gangavaram ◽  
Adarsh Lakkur Siddapa ◽  
Bhanukumar Muthiah ◽  
Dushad Ram
Keyword(s):  
Plasma Lipids ◽  
Therapeutic Option ◽  
Atherosclerotic Plaques ◽  
Obese Patients ◽  
Lifestyle Modifications ◽  
Obese People ◽  
Tnf Α ◽  
Relationship Of ◽  
The Relationship ◽  
Necrosis Factor

Background: Leptin and tumor necrosis factor (TNF­α) are involved in weight regulation1. Elevated lipids are frequently encountered in obese people which are helpful in the formation of atherosclerotic plaques in the coronary arteries. This study helps us to know whether weight neutral antidepressant therapy can be therapeutic option in those with obesity associated with depression.Methods: It is a Longitudinal study of sample size 72 where Patients with obesity attending to JSS hospital who are found to be depressive in both inpatients and out patients fulfilling the inclusion and exclusion criteria.Results: Our study showed mean difference value of weight, BMI and waist circumference, S. leptin, S.TNF-α, S. total cholesterol, S. LDL-C, S. VLDL-C, triglycerides of obese patients treated with lifestyle modifications, psychotherapy and weight neutral antidepressants at baseline and 3rd month was significantly decreased when compared to obese patients treated with lifestyle modifications, psychotherapy alone at baseline and 3rd month is 3.5kgs, 1.2kg/m2, 0.89cm, 9.53pg/ml, 10.86pg/ml, 22.34mg/dl, 17.94mg/dl, 4.42mg/dl, 21.78mg/dl and 1.2kgs, 0.32kg/m2, 0.02cm, 5.22pg/ml, 7.86pg/ml, 11.72mg/dl, 15.37mg/dl, 1.98mg/dl, 9.54mg/dl respectively (p=0.0001).Conclusions: Our study demonstrated a significant weight loss, and significant decrease in S. Leptin, S. TNF- α, TC, LDL-C, VLDL-C, triglycerides, when obese patients treated with lifestyle modifications, psychotherapy and weight neutral antidepressant (Desvenlafaxine).

P742Effects of platelet microparticles on the formation and stability of atherosclerotic plaque in ApoE knockout mice

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Z Wang ◽  
L Pan ◽  
L Chen ◽  
H Hu
Keyword(s):  
Atherosclerotic Plaque ◽  
Blood Lipids ◽  
Inflammatory Factors ◽  
Atherosclerotic Plaques ◽  
High Fat ◽  
Atherosclerotic Plaque Formation ◽  
Tnf Α ◽  
The Stability ◽  
Blood Routine ◽  
Platelet Microparticles

Abstract Background After activation by different factors, platelets can release a large number of platelet microparticles (PMPs), and continue to play a more durable and extensive role in promoting inflammation and thrombosis. Previous studies by our group have shown that PMPs can promote endothelial cell migration and lumen formation in vitro, and promote the release of inflammatory factors from monocytes. However, it is unclear whether PMPs can promote angiogenesis in the plaque and promote vascular wall inflammation and further lead to plaque instability. Purpose To investigate the effect of platelet microparticles (PMPs) from C57BL/6 mice on promoting atherosclerotic plaque formation and plaque stability in ApoE−/− mice. Methods Forty male apolipoprotein E knockout (ApoE−/−) mice, aged 8 weeks and fed for 4 weeks with high-fat diet, were randomly divided into four groups (n=10 in each group)according to the table of random digit. The mice were respectively injected with PBS (PBS group), PMPs-free supernatants (SUP group), low-dose PMPs (LDP group) and high-dose PMPs (HDP group) once a week through tail vein injection for 8 weeks. At the end of the experiment, the mice were euthanized and the blood samples were collected to detect blood routine, blood lipids, liver and kidney function and inflammatory factors including CRP, IL-1β, TNF-α; The aorta and brachiocephalic trunk were sampled to detect the atherosclerotic plaque formation. Oil Red O staining, H&E staining, Masson staining and immunohistochemistry (CD68, MMP-9, α-SMA) were used to examine the stability of the atherosclerotic plaque in each group. Results There were no significant differences in body weight, blood routine (WBC, RBC, PLT, HGB), blood lipids (TG, TCH, LDL, HDL), liver (ALT, AST)and kidney function (UN, Cr)in each group. The levels of serum CRP, IL-1β and TNF-α in LDP group and HDP group were significantly higher than those in PBS group and SUP group (P<0.05). The total area of aortic atherosclerotic plaques in LDP group and HDP group were significantly greater than those in PBS group and SUP group (P<0.05). Compared with the PBS group, the lipid cores of the plaques in the other three groups were significantly increased (P<0.05). The content of collagen and the amount of smooth muscle cells in the plaques were significantly lower in HDP group than in PBS group (P<0.05), while macrophages increased significantly in HDP group (P<0.05). Conclusion PMPs promote the formation of atherosclerotic plaques in high-fat-fed ApoE−/− mice, as well as macrophage infiltration and inflammation in the plaques, reduce the content of collagen and the amount of smooth muscle cells, thus decreasing the stability of plaques.

scholarly journals Phagocytosis of Polymeric Nanoparticles Aided Activation of Macrophages to Induce Atherosclerotic Plaques in Apoe-/- Mice 

2020 ◽  
Author(s):  
Tieying Yin ◽  
Yanhong Li ◽  
Rohmana Maftuhatul Fuad Atik ◽  
Yuzhen Ren ◽  
Fangfang Hu ◽  
...  
Keyword(s):  
Drug Delivery Systems ◽  
Blood Compatibility ◽  
Polymeric Nanoparticles ◽  
Inflammatory Factors ◽  
Atherosclerotic Plaques ◽  
Physiochemical Properties ◽  
Safety Issues ◽  
Tnf Α ◽  
Oil Red O

Abstract The unique physiochemical properties of nanomaterials have been widely used in drug delivery systems and diagnostic contrast agents. The safety issues of biomaterials with exceptional biocompatibility and hemo-compatibility have also received extensive attention at the nanoscale, especially in cardiovascular disease. Therefore, we conducted a study of the effects of poly (lactic-co-glycolic acid) nanoparticles (PLGA NPs) on the development of aortic atherosclerotic plaques in ApoE-/- mice. The particle size of PLGA NPs was 92.69 ± 3.1 nm and the zeta potential were -31.6 ± 2.8 mV, with good blood compatibility. ApoE-/- mice were continuously injected with PLGA NPs intravenously for 4 and 12 weeks. Examination of oil red O stained aortic sinuses confirmed that the accumulation of PLGA NPs promoted the formation of atherosclerotic plaques and increasing the expression of associated inflammatory factors, such as TNF-α, IL-6, and IL-10. The combined exposure of ox-LDL and PLGA NPs accelerated the conversion of macrophages to foam cells. Our results highlight the potential risk for PLGA NPs in vivo and further understanding the interaction between PLGA NPs and the atherosclerotic plaques, which we should consider in future nanomaterial design and pay more attention to the process of using nano-medicines on cardiovascular diseases.

scholarly journals Phagocytosis of polymeric nanoparticles aided activation of macrophages to increase atherosclerotic plaques in ApoE−/− mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Tieying Yin ◽  
Yanhong Li ◽  
Yuzhen Ren ◽  
Atik Rohmana Maftuhatul Fuad ◽  
Fangfang Hu ◽  
...  
Keyword(s):  
Drug Delivery Systems ◽  
Glycolic Acid ◽  
Blood Compatibility ◽  
Polymeric Nanoparticles ◽  
Inflammatory Factors ◽  
Atherosclerotic Plaques ◽  
Physiochemical Properties ◽  
Safety Issues ◽  
Tnf Α ◽  
Oil Red O

AbstractThe unique physiochemical properties of nanomaterials have been widely used in drug delivery systems and diagnostic contrast agents. The safety issues of biomaterials with exceptional biocompatibility and hemo-compatibility have also received extensive attention at the nanoscale, especially in cardiovascular disease. Therefore, we conducted a study of the effects of poly (lactic-co-glycolic acid) nanoparticles (PLGA NPs) on the development of aortic atherosclerotic plaques in ApoE−/− mice. The particle size of PLGA NPs was 92.69 ± 3.1 nm and the zeta potential were − 31.6 ± 2.8 mV, with good blood compatibility. ApoE−/− mice were continuously injected with PLGA NPs intravenously for 4 and 12 weeks. Examination of oil red O stained aortic sinuses confirmed that the accumulation of PLGA NPs caused a significantly higher extension of atherosclerotic plaques and increasing the expression of associated inflammatory factors, such as TNF-α and IL-6. The combined exposure of ox-LDL and PLGA NPs accelerated the conversion of macrophages to foam cells. Our results highlight further understanding the interaction between PLGA NPs and the atherosclerotic plaques, which we should consider in future nanomaterial design and pay more attention to the process of using nano-medicines on cardiovascular diseases.

A Cytochemical Study of Glucose-6-Phosphatase (G-6-PASE) in Cells Participating in Atherogenesis of Rabbit Aorta

1975 ◽  
Vol 33 ◽  
pp. 460-461
Author(s):  
Sidney D. Kobernick ◽  
Edna A. Elfont ◽  
Neddra L. Brooks
Keyword(s):  
Lipid Metabolism ◽  
New Zealand ◽  
Aortic Wall ◽  
Rabbit Aorta ◽  
Plaque Formation ◽  
Metabolic Changes ◽  
Atherosclerotic Plaques ◽  
Cytochemical Study ◽  
Cellular Alteration ◽  
New Zealand White Rabbits

This cytochemical study was designed to investigate early metabolic changes in the aortic wall that might lead to or accompany development of atherosclerotic plaques in rabbits. The hypothesis that the primary cellular alteration leading to plaque formation might be due to changes in either carbohydrate or lipid metabolism led to histochemical studies that showed elevation of G-6-Pase in atherosclerotic plaques of rabbit aorta. This observation initiated the present investigation to determine how early in plaque formation and in which cells this change could be observed.Male New Zealand white rabbits of approximately 2000 kg consumed normal diets or diets containing 0.25 or 1.0 gm of cholesterol per day for 10, 50 and 90 days. Aortas were injected jin situ with glutaraldehyde fixative and dissected out. The plaques were identified, isolated, minced and fixed for not more than 10 minutes. Incubation and postfixation proceeded as described by Leskes and co-workers.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

MAPK's contribute to TNF-α dependent IL-8 secretion indipendently of NF-κB through a post-transcriptional mechanism

2001 ◽  
Vol 120 (5) ◽  
pp. A189-A189
Author(s):  
H JIJON ◽  
W PANENKA ◽  
H PARSONS
Keyword(s):  
Tnf Α

A PPARψ agonist improved diabetic state via decreasing TNF-α without any change including obesity in genetically obese diabetic rats

2001 ◽  
Vol 120 (5) ◽  
pp. A674-A674 ◽  
Author(s):  
A FUNAKOSHI ◽  
M ICHIKAWA ◽  
Y SATO ◽  
S KANAI ◽  
M OHTA ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Diabetic State ◽  
Tnf Α ◽  
Obese Diabetic Rats

Role of cytokines in caerulein-induced acute pancreatilis of IL-1, IL-6 and TNF-α knockoul mice

2001 ◽  
Vol 120 (5) ◽  
pp. A541-A541
Author(s):  
K KITAMURA ◽  
J NIIKAWA ◽  
T IMAMURA ◽  
A TAKAHASHI ◽  
A IKEGAMI ◽  
...  
Keyword(s):  
Tnf Α
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