Abstract 13480: High Density Lipoprotein Promotes Angiogenesis by Suppressing Mir-24-3p Expression

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Zhijun OU ◽  
Hua-Ming Li ◽  
Zhi-Wei Mo ◽  
Yue-Ming Peng ◽  
Yan Li ◽  
...  

Introduction: Previous studies showed that high density lipoprotein (HDL) can stimulate angiogenesis. However, the mechanisms by which HDL promotes angiogenesis remains unclear. Hypothesize: HDL may promote angiogenesis by regulating miRNAs expression. Methods: HDL was isolated from healthy subjects. Human umbilical vein endothelial cells (HUVECs) were cultured with vehicle or HDL (100 μg/ml), and the differential miRNAs expression were indentified by miRNA array and verified by qRT-PCR. HUVECs were treated with vehicle or HDL (100 μg/ml) with or without miRNAs mimic, endothelial cells proliferation, migration and tube formation were detected. The production of nitric oxide(NO) was measured. The expression and phosphorylation of endothelial nitric oxide synthase (eNOS) was determined. Results: The miRNAs profile of HDL-treated HUVECs is significantly different from control group. HDL significantly downregulated miR-24-3p expression. HDL significantly promoted HUVECs proliferation, migration and tube formation. HDL also significantly stimulated NO production and up-regulated the expression and phosphorylation of eNOS. However, HDL did not stimulated HUVECs proliferation, migration, tube formation and NO production as well as the expression and phosphorylation of eNOS after pretreated with miR-24-3p mimic. Conclusions: HDL can promote angiogenesis by suppressing miR-24-3p expression.

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.


2021 ◽  
Vol 22 (19) ◽  
pp. 10287
Author(s):  
Chih-Hsien Wu ◽  
Yi-Lin Chiu ◽  
Chung-Yueh Hsieh ◽  
Guo-Shiang Tsung ◽  
Lian-Shan Wu ◽  
...  

Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilostazol. Human umbilical vein endothelial cells (HUVECs) were cultured with various concentrations of cilostazol to verify its impact on endothelial cells. KLF2, silent information regulator transcript-1 (SIRT1), endothelial nitric oxide synthase (eNOS), and endothelial thrombomodulin (TM) expression levels were examined. We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion. The activation was regulated by SIRT1, which was also stimulated by cilostazol. These findings suggest that cilostazol may be capable of an antithrombotic and vasculoprotective effect in endothelial cells.


2021 ◽  
Vol 34 (1) ◽  
pp. 139-146
Author(s):  
Elham K. Nasser ◽  
Kithar R. Majeed ◽  
Hayder I. Ali

Fortified milk containing Lactobacillus plantarum, L. casei, and L. acidophilus isolates and their mixture were used in dosing the male albino rats at an age of 9-12 weeks at an average of 23 g with induced hypothyroidism at a concentration of 0.6 g.kg-1 of carbimazole. Total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) were estimated. The results showed a significant increase in the level of triglycerides (TG), cholesterol and triglycerides. Low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL), with a significant decrease in the level of high-density lipoprotein (HDL) in infected male mice, compared to the control sample, and upon dosing with liquid milk fortified, it returned to its normal level without significant differences from the control group.


2018 ◽  
Vol 96 (6) ◽  
pp. 713-725 ◽  
Author(s):  
Mabrouk Attia Abd Eldaim ◽  
Fatma Mohamed Ibrahim ◽  
Saher Hassan Orabi ◽  
Azza Hassan ◽  
Hesham Saad El Sabagh

In this study, we evaluated the possible mechanisms through which l-carnitine ameliorates the adverse effects from obesity in rats, induced with a high-fat diet (HFD). For this, 56 albino Wister rats were randomly assigned to 7 groups. The control group was fed a basal diet and injected with saline. The second group was fed the basal diet and injected with l-carnitine (200 mg/kg body mass, by intraperitoneal injection; i.p.). The third group were fed the HFD. The fourth group was fed the HFD and injected with l-carnitine (200 mg/kg body mass, i.p.) for 8 weeks. The fifth group was fed the HFD for 10 weeks. The sixth group were fed the HFD for 10 weeks and were also injected with l-carnitine (200 mg/kg body mass, i.p.) during the final 2 weeks. The seventh group was fed the HFD diet for 8 weeks then the basal diet for 2 weeks. The HFD induced significantly increased levels of hyperglycemia, lipid peroxidation, pathological changes, TNF-α and TGF-β1 protein expression in hepatic tissue, food intake, body weight gain, serum levels of total and non-high-density lipoprotein cholesterol, ketone bodies, triacylglycerol, urea, creatinine, AST, and ALT. However, the HFD diet significantly decreased serum levels of high-density lipoprotein (HDL) and hepatic levels of reduced glutathione. l-Carnitine ameliorated the effects of the HFD on the above-mentioned parameters. This study indicated that l-carnitine had protective and curative effects against HFD-induced hepatosteatosis by reducing hepatic oxidative stress and protein expression of TNF-α and TGF-β1.


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