Effect of Daxx on cholesterol accumulation in hepatic cells

Tuo, Qin-Hui; Liang, Lin; Zhu, Bing-Yang; Cao, Xuan; Liao, Duan‐Fang

doi:10.3748/wjg.14.435

Cited by 7 publications

(5 citation statements)

References 29 publications

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“…We found that curcumin inhibited ox-LDL-induced cholesterol accumulation in cultured VSMCs by increasing caveolin-1 expression via inhibition of the nuclear translocation of SREBP-1 [55] . Furthermore, Daxx mediates oxidized low-density lipoprotein-induced cholesterol accumulation in macrophages and hepatocytes by downregulating SREBP-1 and upregulating caveolin-1 [56,57] .…”

Section: Srebpsmentioning

confidence: 99%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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Cholesterol efflux from lipid-loaded cells is a key athero-protective event that counteracts cholesterol uptake. The imbalance between cholesterol efflux and uptake determines the prevention or development of atherosclerosis. Many proteins and factors participate in the cholesterol efflux event. However, there are currently no systematic models of reverse cholesterol transport (RCT) that include most RCT-related factors and events. On the basis of recent research findings from other and our laboratories, we propose a novel model of one center and four systems with coupling transportation and networking regulation. This model represents a common way of cholesterol efflux; however, the systems in the model consist of different proteins/factors in different cells. In this review, we evaluate the novel model in vascular smooth muscle cells (VSMCs) and macrophages, which are the most important original cells of foam cells. This novel model consists of 1) a caveolae transport center, 2) an intracellular trafficking system of the caveolin-1 complex, 3) a transmembrane transport system of the ABC-A1 complex, 4) a transmembrane transport system of the SR-B1 complex, and 5) an extracelluar trafficking system of HDL/Apo-A1. In brief, the caveolin-1 system transports cholesterol from intracellular compartments to caveolae. Subsequently, both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to extracellular HDL/Apo-A1. The four systems are linked by a regulatory network. This model provides a simple and concise way to understand the dynamic process of atherosclerosis.

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Section: Srebpsmentioning

confidence: 99%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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“…Nuclei were counterstained with DAPI in blue. Apoptosis was quantified by counting TUNELpositive cells per 100 DAPI cells [9] .…”

Section: Tunel Assaymentioning

confidence: 99%

Angiopoietin-1 protects myocardial endothelial cell function blunted by angiopoietin-2 and high glucose condition

et al. 2010

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Aim: To evaluate the effects of angiopoietin-1 (Ang-1) on myocardial endothelial cell function under high glucose (HG) condition. Methods: Mouse heart myocardial endothelial cells (MHMECs) were cultured and incubated under HG (25 mmol/L) or normal glucose (NG, 5 mmol/L) conditions for 72 h. MTT was used to determine cellular viability, and TUNEL assay and caspase-3 enzyme linked immunosorbent assays were used to assay endothelial apoptosis induced by serum starvation. Immunoprecipitation and western blot analysis were used to analyze protein phosphorylation and expression. Endothelial tube formation was used as an in vitro assay for angiogenesis. Results: Exposure of MHMECs to HG resulted in dramatic decreases in phosphorylation of the Tie-2 receptor and its downstream signaling partners, Akt/eNOS, compared to that under NG conditions. Ang-1 (250 ng/mL) increased Tie-2 activation, inhibited cell apoptosis, and promoted angiogenesis. Ang-1-mediated protection of endothelial function was blunted by Ang-2 (25 ng/mL). Conclusion: Ang-1 activates the Tie-2 pathway and restores hyperglycemia-induced myocardial microvascular endothelial dysfunction. This suggests a protective role of Ang-1 in the ischemic myocardium, particularly in hearts affected by hyperglycemia or diabetes.

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“…Terminal Deoxynucleotidyl Transferase-Mediated dUTP Nick End Labeling (TUNEL) Assay As previously reported by Tuo et al [12], cardiac myocytes were cultured for 0, 24, 48, and 72 h and then transferred to two-well chamber slides with a cell density of 2 9 10 5 cells/ml/well. Cardiac myocytes were attached to the slides after 0, 24, 48, and 72 h and were cultured in serum-free media for 0, 24, 48, and 72 h in the presence or absence of infrasound.…”

Section: Neonatal Rat Cardiac Myocytes Culturementioning

confidence: 99%

“…Rats exposed to 8 Hz at 120 dB for up to 45 days showed myocardial cell pathology, microcirculation disturbances, ischemia, and mitochondrial destruction in capillaries [6]. Similarly, rats exposed to [10][11][12][13][14][15] Hz at 135-145 dB for 45 days showed arterial constriction, nuclear deformation, and mitochondrial damage [7]. Recently, we reported infrasound-induced hemodynamics and ultrastructure damages in the rat myocardium [8].…”

Section: Introductionmentioning

confidence: 97%

Infrasound Exposure Induces Apoptosis of Rat Cardiac Myocytes by Regulating the Expression of Apoptosis-Related Proteins

et al. 2011

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It has been reported that exposure to infrasound causes cardiac dysfunction. Allowing for the key role of apoptosis in the pathogenesis of cardiovascular diseases, the objective of this study was to investigate the apoptotic effects of infrasound. Cardiac myocytes cultured from neonatal rats were exposed to infrasound of 5 Hz at 130 dB. The apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Also, the expression levels of a series of apoptosis-related proteins were detected. As a result, infrasound induced apoptosis of cultured rat cardiac myocytes in a time-dependant manner. The expression of proapoptotic proteins such as Bax, caspase-3, caspase-8, caspase-9, and FAS was significantly up-regulated, with concomitant down-regulated expression of antiapoptotic proteins such as Bcl-x, and the inhibitory apoptosis proteins family proteins including XIAP, cIAP-1, and cIAP-2. The expression of poly (ADP-ribose) polymerase and β-catenin, which are the substrate proteins of caspase-3, was significantly decreased. In conclusion, infrasound is an apoptotic inducer of cardiac myocytes.

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Effect of Daxx on cholesterol accumulation in hepatic cells

Cited by 7 publications

References 29 publications

A novel model of cholesterol efflux from lipid-loaded cells

A novel model of cholesterol efflux from lipid-loaded cells

Angiopoietin-1 protects myocardial endothelial cell function blunted by angiopoietin-2 and high glucose condition

Infrasound Exposure Induces Apoptosis of Rat Cardiac Myocytes by Regulating the Expression of Apoptosis-Related Proteins

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