Human high-density lipoprotein microtranscriptome is unique and suggests an extended role in lipid metabolism

Epigenomics ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 917-934 ◽  
Author(s):  
Véronique Desgagné ◽  
Renée Guérin ◽  
Simon-Pierre Guay ◽  
Marjorie Boyer ◽  
Elizabeth Hutchins ◽  
...  
1986 ◽  
Vol 261 (21) ◽  
pp. 9644-9651 ◽  
Author(s):  
G A Coetzee ◽  
A F Strachan ◽  
D R van der Westhuyzen ◽  
H C Hoppe ◽  
M S Jeenah ◽  
...  

Author(s):  
Huijun Chen ◽  
Jing Gao ◽  
Qian Xu ◽  
Dongmei Wan ◽  
Wenji Zhai ◽  
...  

The present study aims to explore the role of microRNA 145-5p (miR-145-5p) in hyperlipidemia. Using bioinformatics tools and a wide range of function and mechanism assays, we attempted to understand the specific function and potential mechanism of miR-145-5p in hyperlipidemia. A cholesterol-enriched diet induced an increase of serum cholesterol and triacylglycerol but a decrease of serum high-density lipoprotein. MiR-145-5p level was decreased in hyperlipidemia rat models. MiR-145-5p regulated lipid metabolism by antagonizing the alteration of high-density lipoprotein, cholesterol, and triacylglycerol in serum mediated by a cholesterol-enriched diet. In mechanism, miR-145-5p directly bound with p21 protein (RAC1)-activated kinase 7 (PAK7) and negatively regulated mRNA and protein levels of PAK7 in THP-1 cells. Furthermore, miR-145-5p level was negatively associated with PAK7 level in rat cardiac tissues. Finally, overexpression of PAK7 reversed the effects of miR-145-5p on β-catenin activation and M2 macrophages polarization in THP-1 cells. In conclusion, MiR-145-5p modulated lipid metabolism and M2 macrophage polarization by targeting PAK7 and regulating β-catenin signaling in hyperlipidemia, which may provide a potential biomarker for the treatment of hyperlipidemia-induced cardiovascular diseases.


2014 ◽  
Vol 27 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Francisca das Chagas do Amaral Souza ◽  
Nadja Pinto Garcia ◽  
Rejane Souza de Aquino Sales ◽  
Jaime Paiva Lopes Aguiar ◽  
Wallice Luiz Paxiúba Duncan ◽  
...  

OBJECTIVE: The present study aimed to evaluate the effect of feeding diets enriched with fatty fish from the Amazon basin on lipid metabolism. METHODS: Male Wistar rats were divided into four groups: control group treated with commercial chow; Mapará group was fed diet enriched with Hypophthalmus edentatus; Matrinxã group was fed diet enriched with Brycon spp.; and, Tambaqui group was fed diet enriched with Colossoma macropomum. Rats with approximately 240g±0.60 of body weight were fed ad libitum for 30 days, and then were sacrificed for collection of whole blood and tissues. RESULTS: The groups treated with enriched diets showed a significant reduction in body mass and lipogenesis in the epididymal and retroperitoneal adipose tissues and carcass when compared with the control group. However, lipogenesis in the liver showed an increase in Matrinxã group compared with the others groups. The levels of serum triglycerides in the treated groups with Amazonian fish were significantly lower than those of the control group. Moreover, total cholesterol concentration only decreased in the group Matrinxã. High Density Lipoprotein cholesterol levels increased significantly in the Mapará and Tambaqui compared with control group and Matrinxã group. The insulin and leptin levels increased significantly in all treatment groups. CONCLUSION: This study demonstrated that diets enriched with fatty fish from the Amazon basin changed the lipid metabolism by reducing serum triglycerides and increasing high density lipoprotein-cholesterol in rats fed with diets enriched with Mapará, Matrinxã, and Tambaqui.


2006 ◽  
Vol 5 (8) ◽  
pp. 1276-1286 ◽  
Author(s):  
Sara D. Faulkner ◽  
Monika W. Oli ◽  
Rudo Kieft ◽  
Laura Cotlin ◽  
Justin Widener ◽  
...  

ABSTRACT The host range of African trypanosomes is influenced by innate protective molecules in the blood of primates. A subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I, apolipoprotein L-I, and haptoglobin-related protein is toxic to Trypanosoma brucei brucei but not the human sleeping sickness parasite Trypanosoma brucei rhodesiense. It is thought that T. b. rhodesiense evolved from a T. b. brucei-like ancestor and expresses a defense protein that ablates the antitrypanosomal activity of human HDL. To directly investigate this possibility, we developed an in vitro selection to generate human HDL-resistant T. b. brucei. Here we show that conversion of T. b. brucei from human HDL sensitive to resistant correlates with changes in the expression of the variant surface glycoprotein (VSG) and abolished uptake of the cytotoxic human HDLs. Complete transcriptome analysis of the HDL-susceptible and -resistant trypanosomes confirmed that VSG switching had occurred but failed to reveal the expression of other genes specifically associated with human HDL resistance, including the serum resistance-associated gene (SRA) of T. b. rhodesiense. In addition, we found that while the original active expression site was still utilized, expression of three expression site-associated genes (ESAG) was altered in the HDL-resistant trypanosomes. These findings demonstrate that resistance to human HDLs can be acquired by T. b. brucei.


1981 ◽  
Vol 98 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Thomas Rådberg ◽  
Anders Gustafson ◽  
Asbjörn Skryten ◽  
Kirsten Karlsson

Abstract. Thirtyeight women with insulin-dependent diabetes were randomly allocated to contraception with either a progestogen only (Lynestrenol 0.5 mg daily) (LYN), a combined oral contraceptive (OC) (Ethinyl oestradiol 50 μg + Lynestrenol 2.5 mg) (EE + LYN) or a non-hormonal intrauterine device (IUD). Diabetes control (i.e. insulin dosage, blood and urinary glucose and body weight) and the lipid concentration in serum and in high density lipoprotein (HDL) were assessed before and during six months use of the respective contraceptives. In the LYN group urinary glucose excretion increased 10% in spite of unchanged blood glucose, body weight and insulin requirement. All serum lipids decreased; triglycerides by 40% (P < 0.01), cholesterol by 13% (P < 0.01) and phospholipids by 12% (P = 0.06), without alteration of HDL lipids. In the group using combined OC (EE + LYN) the insulin requirement increased by 7% (P < 0.01) without any change in body weight or blood and urinary glucose. Serum as well as HDL lipids remained unchanged. In the IUD group neither diabetes control nor serum or HDL lipids were altered. It is concluded that in insulin-dependent diabetics the progestogen (LYN) has little influence on diabetes control but has a marked, though probably not adverse, effect on lipid metabolism. The combined OC (EE + LYN) may impair glucose homeostasis slightly but has little influence on serum or HDL lipids. These findings seem to differ from those obtained in non-diabetics during administration of contraceptive steroids and these differences suggest that absence of endogenous insulin production enhances the effects of progestogen and reduces the effects of synthetic oestrogens on lipid metabolism.


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