scholarly journals Profile of circulating MicroRNAs in low density lipoprotein uptake: literature review

2021 ◽  
Vol 13 (1) ◽  
pp. e4546
Author(s):  
Maria Elisabete Silva Santos ◽  
Ricardo Sousa de Oliveira Paraense ◽  
Ricardo Roberto de Souza Fonseca ◽  
Danilo Leôncio Aguiar Pereira ◽  
Carlos Eduardo Silva Cordeiro ◽  
...  

Objective: Delineate a profile of circulating miRNA that interfere with the uptake of c-LDL through the regulation of LDL, APOB-100 and PCSK9 genes that can be used as biomarkers for prognosis and treatment of atherosclerosis. Bibliography review: The atherosclerosis, a chronic and inflammatory disease that occurs when there are high levels of LDL on plasma. This important risk factor for development of cardiovascular disease is the main cause of death worldwide. The miRNAs have recently emerged as potential biomarkers and therapeutic target for lipid metabolism disorders. In this review, we will provide profile of circulating miRNAs that have demonstrated being regulators of PCSK9, LDL and APOB100 genes. Recent work has identified the miR-148, miR-128, miR-27a/b, miR-185, miR-301, miR-130 as important regulators of this pathway because they decrease supply of LDL receptors through interaction with PCSK9. Final considerations: We conclude that, when overexpressed, miR-148a, mir128 and miR-27a/b, miR-122 and miR-34 are related to decrease in LDL, facilitating occurrence of atherosclerosis. Detection of miRNAs profile could be used in the future as a biomarker for disturbs linked to c-LDL uptake and in future anti-miRNAs therapies may be used in the treatment of atherosclerosis.

Author(s):  
Maria Elisabete Silva Santos ◽  
Ricardo Sousa De Oliveira Paraense ◽  
Eric Artur Cortinhas-Alves ◽  
Danilo Leôncio Aguiar Pereira

The atherosclerosis, a chronic and inflammatory disease that occurs when there are high levels of low-density lipoprotein (LDL) on plasma. This important risk factor for development of cardiovascular disease (CVD) is the main cause of death worldwide. MicroRNAs have recently emerged as potential biomarkers and therapeutic target for lipid metabolism disorders. In this review, we will provide profile of surrounding miRNAs that have demonstrated being regulators of PCSK9, LDLR and APOB100 genes. Recent work has identified the mir-148, mir-128, mir-27a/b, mir-185, mir-301, mir-130 as important regulators of this pathway because they decrease supply of LDL receptors through interaction with PCSK9. Inhibition of LDLR expression cause elevation of plasma LDL levels which induces atherosclerosis. While mir-30c, mir-122, mir-34 decrease MTTP, which promotes degradation of APOB100 preventing assembly and secretion of VLDL. We conclude that, when overexpressed, mir-148a, mir128 and mir-27a/b, mir-122 and mir-34 are related to decrease in LDLR, facilitating occurrence of atherosclerosis. While mir-30 has been linked to decreased atherosclerosis. Detection of miRNAs profile could be used in the future as a biomarker for disturbs linked to c-LDL uptake and in future anti-miRNAs therapies may be used in the treatment of atherosclerosis.


1985 ◽  
Vol 79 (1) ◽  
pp. 317-325
Author(s):  
J. Gaffney ◽  
D. West ◽  
F. Arnold ◽  
A. Sattar ◽  
S. Kumar

Acetylated low density lipoprotein (Ac-LDL) is taken up by bovine aortic and adrenal capillary cells but not by brain capillary cells. This indicates that the uptake of Ac-LDL is not a feature of all types of endothelial cell. A quantitative examination of lipoprotein uptake by flow cytometry showed cells in G2M took up 45% more Ac-LDL than those in G1S. Compared with confluent cultures, sub-confluent bovine aortic cells took up three times as much LDL but Ac-LDL uptake was increased by only 34%. This indicates that the Ac-LDL receptor is not down-regulated to the same extent as that for LDL.


2021 ◽  
Vol 556 ◽  
pp. 192-198
Author(s):  
Ryo Ninomiya ◽  
Shuichi Kubo ◽  
Takehiro Baba ◽  
Tooru Kajiwara ◽  
Akinori Tokunaga ◽  
...  

1979 ◽  
Vol 83 (3) ◽  
pp. 588-594 ◽  
Author(s):  
H S Kruth ◽  
J Avigan ◽  
W Gamble ◽  
M Vaughan

The effect of cell density on low density lipoprotein (LDL) binding by cultured human skin fibroblasts was investigated. Bound LDL was visualized by indirect immunofluorescence. Cellular lipid and cholesterol were monitored by fluorescence in cells stained with phosphine 3R and filipin, respectively. LDL binding and lipid accumulation were compared in cells in stationary and exponentially growing cultures, in sparsely and densely plated cultures, in wounded and non-wounded areas of stationary cultures, and in stationary cultures with and without the addition of lipoprotein-deficient serum. We conclude that LDL binding and cholesterol accumulation induced by LDL are influenced by cell density. It appears that, compared to rapidly growing cells, quiescent (noncycling) human fibroblasts exhibit fewer functional LDL receptors.


1986 ◽  
Vol 6 (9) ◽  
pp. 3268-3277
Author(s):  
R D Sege ◽  
K F Kozarsky ◽  
M Krieger

The ldlA locus is one of four Chinese hamster ovary (CHO) cell loci which are known to be required for the synthesis of functional low-density lipoprotein (LDL) receptors. Previous studies have suggested that the ldlA locus is diploid and encodes the LDL receptor. To confirm this assignment, we have isolated a partial genomic clone of the Chinese hamster LDL receptor gene and used this and other nucleic acid and antibody probes to study a family of ldlA mutants isolated after gamma-irradiation. Our analysis suggests that there are two LDL receptor alleles in wild-type CHO cells. Each of the three mutants isolated after gamma-irradiation had detectable deletions affecting one of the two LDL receptor alleles. One of the mutants also had a disruption of the remaining allele, resulting in the synthesis of an abnormal receptor precursor which was not subject to Golgi-associated posttranslational glycoprotein processing. The correlation of changes in the expression, structure, and function of LDL receptors with deletions in the LDL receptor genes in these mutants directly demonstrated that the ldlA locus in CHO cells is diploid and encodes the LDL receptor. In addition, our analysis suggests that CHO cells in culture may contain a partial LDL receptor pseudogene.


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