Updates on apolipoprotein CIII

Zheng, Changjie

doi:10.1097/mol.0000000000000040

Cited by 47 publications

(14 citation statements)

References 44 publications

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“…There are no data about the relationship between apoCIII and MPO or PON1 in HDL. Our results show for the first time that apoCIII is increased in HDL 2 and HDL 3 (HDL 2 > HDL 3 ) from ACS compared to SA and N. The higher levels of apoCIII in HDL 2 compared to HDL 3 could be associated with the higher content of TG in HDL 2 versus HDL 3 , as was previously reported 41 . It is known that functional HDL inhibit or attenuate the oxidation of LDL and of the membrane phospholipids 18 , 42 .…”

Section: Discussionsupporting

confidence: 85%

Dysfunctional high-density lipoproteins have distinct composition, diminished anti-inflammatory potential and discriminate acute coronary syndrome from stable coronary artery disease patients

Carnuta

Stancu

Toma

et al. 2017

Sci Rep

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There is a stringent need to find means for risk stratification of coronary artery diseases (CAD) patients. We aimed at identifying alterations of plasma high-density lipoproteins (HDL) components and their validation as dysfunctional HDL that could discriminate between acute coronary syndrome (ACS) and stable angina (SA) patients. HDL2 and HDL3 were isolated from CAD patients’ plasma and healthy subjects. ApolipoproteinAI (apoAI), apoAII, apoCIII, malondialdehyde (MDA), myeloperoxidase (MPO), ceruloplasmin and paraoxonase1 (PON1) were assessed. The anti-inflammatory potential of HDL subfractions was tested by evaluating the secreted inflammatory molecules of tumor necrosis factor α-activated endothelial cells (EC) upon co-incubation with HDL2 or HDL3. We found in ACS versus SA patients: 40% increased MPO, MDA, apoCIII in HDL2 and HDL3, 35% augmented apoAII in HDL2, and in HDL3 increased ceruloplasmin, decreased apoAII (40%) and PON1 protein and activity (15% and 25%). Co-incubation of activated EC with HDL2 or HDL3 from CAD patients induced significantly increased levels of secreted inflammatory molecules, 15–20% more for ACS versus SA. In conclusion, the assessed panel of markers correlates with the reduced anti-inflammatory potential of HDL subfractions isolated from ACS and SA patients (mostly for HDL3 from ACS) and can discriminate between these two groups of CAD patients.

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Section: Discussionsupporting

confidence: 85%

Dysfunctional high-density lipoproteins have distinct composition, diminished anti-inflammatory potential and discriminate acute coronary syndrome from stable coronary artery disease patients

Carnuta

Stancu

Toma

et al. 2017

Sci Rep

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“…There are data indicating that apo C3 directly provokes proinflammatory responses in vascular cells, including monocytes and endothelial cells. 31,32 The findings on association between circulating levels of PTX3 and measures of adiposity are inconsistent: some studies have found positive, whereas other have demonstrated inverse associations. [33][34][35] In our patients with T2D without NAFLD, positive association between PTX3 and waist circumference and BMI was found, while, interestingly, in patients with NAFLD such association did not occur.…”

Section: Discussionmentioning

confidence: 99%

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Trojak¹,

Waluś-Miarka²,

Kapusta³

et al. 2019

Polish Archives of Internal Medicine

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INTRODUCTION Nonalcoholic fatty liver disease (NAFLD) is common in patients with type 2 diabetes (T2D). Pentraxin 3 (PTX3), a marker of inflammation, is a cardiovascular risk factor. OBJECTIVES We examined clinical and biochemical factors associated with serum PTX3 concentrations in patients with T2D with and without NAFLD. PATIENTS AND METHODS Serum material was obtained from 116 patients with T2D (mean age, 59.1 years), including 79 patients with NAFLD. RESULTS Median (interquartile range) PTX3 level was 4.264 (2.293) ng/ml in patients with and 3.773 (3.223) ng/ml in patients without NAFLD (P = 0.93). In the whole group, PTX3 level was associated with total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein (apo) B100, apo C3, triglyceride (TG) concentrations, and waist circumference after adjustment for age and gender. As indicated by partial regression coefficient b, increase of independent variable LDL-C by 1 mmol/l was associated with the rise of PTX3 by 1.2017 ng/ml, increase of apo B100 by 1 mg/dl with the rise of PTX3 by 1.0051 ng/ml, and increase of apo C3 by 1 µg/dl with the rise of PTX3 by 1.0012 ng/ml. In patients with T2D with NAFLD, total cholesterol, LDL-C, TG, apo C3, and apo B100 were associated with PTX3. Associations of PTX3 with apolipoproteins were observed only in the NAFLD group. CONCLUSIONS Reported associations of PTX3 level add new insight into possible mechanisms of its atherogenic actions.

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“…This hypertriglyceridemia-associated systemic inflammation can be reversed to varying degrees by administration of fibrates, resveratrol or omega-3 fatty acids [42–44]. However, independent of triglyceride levels, apoCIII has inflammatory and cytotoxic effects [45]. For instance, purified human apoCIII enhances the attachment of monocyte-like cells to the human saphenous vein or coronary artery endothelial cells under both static and laminar shear stress conditions via induction of VCAM-1 [46].…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein CIII Overexpression‐Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death

Paiva

Raposo

Wanschel

et al. 2017

Oxidative Medicine and Cellular Longevity

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Nonalcoholic fatty liver disease (NAFLD) is the principal manifestation of liver disease in obesity and metabolic syndrome. By comparing hypertriglyceridemic transgenic mice expressing apolipoprotein (apo) CIII with control nontransgenic (NTg) littermates, we demonstrated that overexpression of apoCIII, independent of a high-fat diet (HFD), produces NAFLD-like features, including increased liver lipid content; decreased antioxidant power; increased expression of TNFα, TNFα receptor, cleaved caspase-1, and interleukin-1β; decreased expression of adiponectin receptor-2; and increased cell death. This phenotype is aggravated and additional NAFLD features are differentially induced in apoCIII mice fed a HFD. HFD induced glucose intolerance together with increased gluconeogenesis, indicating hepatic insulin resistance. Additionally, the HFD led to marked increases in plasma TNFα (8-fold) and IL-6 (60%) in apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3), and apoptosis were augmented in apoCIII mice regardless of whether a HFD or a low-fat diet was provided. Fenofibrate treatment reversed several of the effects associated with diet and apoCIII expression but did not normalize inflammatory traits even when liver lipid content was fully corrected. These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.

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Updates on apolipoprotein CIII

Cited by 47 publications

References 44 publications

Dysfunctional high-density lipoproteins have distinct composition, diminished anti-inflammatory potential and discriminate acute coronary syndrome from stable coronary artery disease patients

Dysfunctional high-density lipoproteins have distinct composition, diminished anti-inflammatory potential and discriminate acute coronary syndrome from stable coronary artery disease patients

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Apolipoprotein CIII Overexpression‐Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death

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