scholarly journals Reconstitution of Low-Density Lipoproteins with Fatty Acids for the Targeted Delivery of Drugs into Cancer Cells

2017 ◽  
Vol 56 (35) ◽  
pp. 10399-10402 ◽  
Author(s):  
Chunlei Zhu ◽  
Pallab Pradhan ◽  
Da Huo ◽  
Jiajia Xue ◽  
Song Shen ◽  
...  
2017 ◽  
Vol 129 (35) ◽  
pp. 10535-10538 ◽  
Author(s):  
Chunlei Zhu ◽  
Pallab Pradhan ◽  
Da Huo ◽  
Jiajia Xue ◽  
Song Shen ◽  
...  

2004 ◽  
Vol 10 (24) ◽  
pp. 8275-8283 ◽  
Author(s):  
Iris J. Edwards ◽  
Isabelle M. Berquin ◽  
Haiguo Sun ◽  
Joseph T. O’Flaherty ◽  
Larry W. Daniel ◽  
...  

2021 ◽  
Vol 8 (7) ◽  
pp. 121
Author(s):  
Dongmei Xing ◽  
Baogen Wang ◽  
Hong Lu ◽  
Tao Peng ◽  
Jianming Su ◽  
...  

Fatty liver is closely associated with elevated concentrations of nonesterified fatty acids (NEFA) and a low level of very low-density lipoproteins (VLDL) in blood of dairy cows. High NEFA inhibit the VLDL synthesis and assembly, and cause hepatic triacylglycerol (TAG) deposition. Sirtuin 3 (SIRT3), a mitochondrial deacetylase, antagonizes NEFA-induced TAG accumulation through modulating expressions of fatty acid synthesis and oxidation genes in cow hepatocytes. However, the role of SIRT3 in the VLDL synthesis and assembly was largely unknown. Here we aimed to test whether SIRT3 would recover the synthesis and assembly of VLDL in cow hepatocytes induced by high NEFA. Primary cow hepatocytes were isolated from 3 Holstein cows. Hepatocytes were infected with SIRT3 overexpression adenovirus (Ad-SIRT3), SIRT3-short interfering (si) RNA, or first infected with Ad-SIRT3 and then incubated with 1.0 mM NEFA (Ad-SIRT3 + NEFA). Expressions of key genes in VLDL synthesis and the VLDL contents in cell culture supernatants were measured. SIRT3 overexpression significantly increased the mRNA abundance of microsomal triglyceride transfer protein (MTP), apolipoprotein B100 (ApoB100) and ApoE (p < 0.01), and raised VLDL contents in the supernatants (p < 0.01). However, SIRT3 silencing displayed a reverse effect in comparison to SIRT3 overexpression. Compared with NEFA treatment alone, the Ad-SIRT3 + NEFA significantly upregulated the mRNA abundance of MTP, ApoB100 and ApoE (p < 0.01), and increased VLDL contents in the supernatants (p < 0.01). Our data demonstrated that SIRT3 restored the synthesis and assembly of VLDL in cow hepatocytes challenged with NEFA, providing an in vitro basis for further investigations testing its feasibility against hepatic TAG accumulation in dairy cows during the perinatal period.


Nanoscale ◽  
2021 ◽  
Author(s):  
Chao Wang ◽  
Xianhao Zhao ◽  
Haoyu Jiang ◽  
Jiaxin Wang ◽  
Weixiu Zhong ◽  
...  

Low-density lipoproteins (LDLs) reconstituted with a multifunctional mitochondrion-targeting photosensitizer are able to achieve fluorescence-feedback photodynamic therapy of LDL receptor-overexpressing cancer cells.


2002 ◽  
Vol 283 (2) ◽  
pp. L310-L318 ◽  
Author(s):  
Alan J. Ryan ◽  
Jheem D. Medh ◽  
Diann M. McCoy ◽  
Ronald G. Salome ◽  
Rama K. Mallampalli

We examined whether administration of very low-density lipoproteins (VLDL) to pregnant rats increases surfactant phosphatidylcholine (PtdCho) content in fetal pre-type II alveolar epithelial cells. VLDL-triglycerides are hydrolyzed to fatty acids by lipoprotein lipase (LPL), an enzyme activated by heparin. Fatty acids released by LPL can incorporate into the PtdCho molecule or activate the key biosynthetic enzyme cytidylyltransferase (CCT). Dams were given BSA, heparin, VLDL, or VLDL with heparin intravenously. Radiolabeled VLDL given to the pregnant rat crossed the placenta and was distributed systemically in the fetus and incorporated into disaturated PtdCho (DSPtdCho) in pre-type II cells. Maternal administration of VLDL with heparin increased DSPtdCho content in cells by 45% compared with control ( P < 0.05). VLDL produced a dose-dependent, saturable, and selective increase in CCT activity. VLDL did not significantly alter immunoreactive CCT content but increased palmitic, stearic, and oleic acids in pre-type II cells. Furthermore, hypertriglyceridemic apolipoprotein E knockout mice contained significantly greater levels of DSPtdCho content in alveolar lavage and CCT activity compared with either LDL receptor knockout mice or wild-type controls that have normal serum triglycerides. Thus the nutritional or genetic modulation of serum VLDL-triglycerides provides specific fatty acids that stimulate PtdCho synthesis and CCT activity thereby increasing surfactant content.


1996 ◽  
Vol 84 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Wolfgang Jira ◽  
Gerhard Spiteller ◽  
Axel Schramm

1980 ◽  
Vol 94 (3) ◽  
pp. 503-516 ◽  
Author(s):  
J. E. Storry ◽  
P. E. Brumby ◽  
B. Tuckley ◽  
V. A. Welch ◽  
D. Stead ◽  
...  

SummaryEffects of 0, 1·7, 3·3 or 5·0 kg/day of a protected soya bean – tallow supplement, incorporated into a hay:concentrate diet (25:75) and fed ad libitumto Friesian cows, on intake and digestion of fatty acids, on output of milk fatty acids and on blood lipoprotein composition were measured.Most of the increased intake of fatty acids, approximately 1 kg/day, was accounted for by increased intakes of C16:0, C18:0 and C18:1. At low intakes, amounts of all fatty acids apparently digested were linearly related to their respective intakes. At high intakes of C16 and C18 acids, curvilinear relationships were established.Yield of total milk fat was related positively to dietary intakes of total fatty acid and carbohydrate and negatively to live-weight change. Yields of short and intermediate chain acids in milk, synthesized within the mammary gland, were negatively correlated and yields of C18 fatty acids positively correlated with respective dietary intakes of these acids. Decreased proportions of C4–16 and increased proportions of C18:0 and C18:1 fatty acids in milk were associated with increased protected tallow in the diet. Yields of C16:1 and C18:1 were positively related to corresponding outputs of saturated acids and negatively to weeks of lactation. The proportion of C18:1 in milk was positively related to the corresponding proportion of C18:0.The increased intake of fatty acids resulted in increased concentrations of very low density lipoproteins (VLDL, d < 1·019 g/ml), low density lipoproteins (LDL1 + LDL2, 1·019 < d < 1·06 g/ml), high density lipoproteins (d > 1·060 g/ml) and serum free fatty acids. Most of the increase in low density lipoproteins was accounted for by a very large increase in LDL1, whose proportion increased from 17 to 75% (2 to 22% of total serum lipid). The proportion of triglyceride in the combined low density lipoprotein fraction decreased from 11 to 2% whilst phospholipids increased from 29 to 36%. These changes were attributed to the increased proportion of LDL1 present.The proportions of VLDL and LDL triglyceride taken up by the mammary gland averaged 0·79 and 0·34 respectively. The proportion of VLDL+LDL triglyceride taken up by the gland decreased with increased amounts of fatty acid digested. Yields of C18 fatty acids in milk tended to be positively related to apparent uptakes of VLDL triglyceride and to VLDL C18 fatty acids, but negatively related to apparent uptakes of LDL triglycerides and LDL C18 fatty acids. It is suggested that the increased LDL1 resulted from the utilization of VLDL triglyceride for milk fat formation.Protected lipid feeding increased the proportion of C14:0, C16:0 C16:1 and C18:1 and decreased the proportions of C14:1 and C18:0 fatty acids in jugular serum triglycerides. Similar changes were observed in jugular VLDL triglycerides. Differences in the compositions of VLDL and LDL triglycerides across the mammary gland were observed and attributed either to selective uptake or to interchange of fatty acids between triglycerides and free fatty acids.


1978 ◽  
Vol 176 (1) ◽  
pp. 169-174 ◽  
Author(s):  
P Thomopoulos ◽  
M Berthelier ◽  
D Lagrange ◽  
M J Chapman ◽  
M H Laudat

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.


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