lipoprotein uptake
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2021 ◽  
pp. 395-400
Author(s):  
Mohammad Jalili-Nik ◽  
Khadijeh Mahboobnia ◽  
Paul C. Guest ◽  
Muhammed Majeed ◽  
Khalid Al-Rasadi ◽  
...  

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

2021 ◽  
pp. ASN.2020091376
Author(s):  
Pragyi Shrestha ◽  
Saritha Adepu ◽  
Romain R. Vivès ◽  
Rana El Masri ◽  
Astrid Klooster ◽  
...  

BackgroundDyslipidemia is an important risk factor in CKD. The liver clears triglyceride-rich lipoproteins (TRL) via LDL receptor (LDLR), LDLR-related protein-1 (LRP-1), and heparan sulfate proteoglycans (HSPGs), mostly syndecan-1. HSPGs also facilitate LDLR degradation by proprotein convertase subtilisin/kexin type 9 (PCSK9). Progressive renal failure affects the structure and activity of hepatic lipoprotein receptors, PCSK9, and plasma cholesterol.MethodsUninephrectomy- and aging-induced CKD in normotensive Wistar rats and hypertensive Munich-Wistar-Frömter (MWF) rats.ResultsCompared with 22-week-old sex- and strain-matched rats, 48-week-old uninephrectomized Wistar-CKD and MWF-CKD rats showed proteinuria, increased plasma creatinine, and hypercholesterolemia (all P<0.05), which were most apparent in hypertensive MWF-CKD rats. Hepatic PCSK9 expression increased in both CKD groups (P<0.05), with unusual sinusoidal localization, which was not seen in 22-week-old rats. Heparan sulfate (HS) disaccharide analysis, staining with anti-HS mAbs, and mRNA expression of HS polymerase exostosin-1 (Ext-1), revealed elongated HS chains in both CKD groups. Solid-phase competition assays showed that the PCSK9 interaction with heparin-albumin (HS-proteoglycan analogue) was critically dependent on polysaccharide chain length. VLDL binding to HS from CKD livers was reduced (P<0.05). Proteinuria and plasma creatinine strongly associated with plasma cholesterol, PCSK9, and HS changes.ConclusionsProgressive CKD induces hepatic HS elongation, leading to increased interaction with PCSK9. This might reduce hepatic lipoprotein uptake and thereby induce dyslipidemia in CKD. Therefore, PCSK9/HS may be a novel target to control dyslipidemia.


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.


ACS Nano ◽  
2020 ◽  
Author(s):  
Staffan Hildebrand ◽  
Norbert Löwa ◽  
Hendrik Paysen ◽  
Raluca M. Fratila ◽  
Laia Reverte-Salisa ◽  
...  

2020 ◽  
Vol 295 (14) ◽  
pp. 4673-4683 ◽  
Author(s):  
Isao Tamura ◽  
Haruka Takagi ◽  
Yumiko Doi-Tanaka ◽  
Yuichiro Shirafuta ◽  
Yumiko Mihara ◽  
...  

We previously reported that the transcription factor Wilms tumor 1 (WT1) regulates the expression of insulin-like growth factor-binding protein-1 (IGFBP-1) and prolactin (PRL) during decidualization of human endometrial stromal cells (ESCs). However, other roles of WT1 in decidualization remain to be fully clarified. Here, we investigated how WT1 regulates the physiological functions of human ESCs during decidualization. We incubated ESCs isolated from proliferative-phase endometrium with cAMP to induce decidualization, knocked down WT1 with siRNA, and generated three types of treatments (nontreated cells, cAMP-treated cells, and cAMP-treated + WT1-knockdown cells). To identify WT1-regulated genes, we used gene microarrays and compared the transcriptome data obtained among these three treatments. We observed that WT1 up-regulates 121 genes during decidualization, including several genes involved in lipid transport. The WT1 knockdown inhibited lipid accumulation (LA) in the cAMP-induced ESCs. To examine the mechanisms by which WT1 regulates LA, we focused on very low-density lipoprotein receptor (VLDLR), which is involved in lipoprotein uptake. We found that cAMP up-regulates VLDLR and that the WT1 knockdown inhibits it. Results of ChIP assays revealed that cAMP increases the recruitment of WT1 to the promoter region of the VLDLR gene, indicating that WT1 regulates VLDLR expression. Moreover, VLDLR knockdown inhibited cAMP-induced LA, and VLDLR overexpression reverted the suppression of LA caused by the WT1 knockdown. Taken together, our results indicate that WT1 enhances lipid storage by up-regulating VLDLR expression in human ESCs during decidualization.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Fabio Michelet ◽  
Aishwarya Balasankar ◽  
Nickolas Teo ◽  
Lawrence W. Stanton ◽  
Shweta Singhal

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