High-Density Lipoprotein (HDL): The Role of Reverse Cholesterol Transport in Human Health and Disease – 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (25 April 2022) | Viewed by 2604

Special Issue Editor


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Guest Editor
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-8830, USA
Interests: elucidating the role of HDL and reverse cholesterol transport in atheroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

After the success of the first edition of the Special Issue on “High-Density Lipoprotein (HDL): The Role of Reverse Cholesterol Transport in Human Health and Disease” in 2020, it is our pleasure to announce a new edition on the same topic.

Although high-density lipoprotein (HDL) cholesterol levels continue to be included in cardiovascular risk assessment tools, findings from genetic studies and various pharmacologic interventions have called into question the causal role of HDL cholesterol in atherosclerotic heart disease and the suitability of HDL cholesterol as a treatment target. Recent studies have illuminated the dynamic and complex HDL metabolic pathways defined by lipid transport out of the cell, reverse cholesterol transport (RCT), but directly linked to a myriad of other vascular and nonvascular functions. It has become increasingly clear that HDL metabolism has direct relevance to a number of pathophysiologic processes.

I am pleased to announce this Special Issue, which continues to address how HDL and RCT may impact fundamental biologic processes as well as contribute to pathophysiology across a spectrum of human diseases. A major focus of this issue is to structure our current understanding of HDL and RCT by disease process and to emphasize both the fundamental basic science as well as the relevance to human disease.

Dr. Anand K. Rohatgi
Guest Editor

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Keywords

  • high-density lipoprotein (HDL)
  • reverse cholesterol transport
  • atherosclerosis
  • cancer
  • renal disease
  • dementia
  • vascular disease
  • therapy
  • lifestyle
  • macular degeneration

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Published Papers (1 paper)

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Research

12 pages, 987 KiB  
Article
Utilizing the LoxP-Stop-LoxP System to Control Transgenic ABC-Transporter Expression In Vitro
by Ikechukwu Esobi, Olanrewaju Oladosu, Jing Echesabal-Chen and Alexis Stamatikos
Biomolecules 2022, 12(5), 679; https://doi.org/10.3390/biom12050679 - 8 May 2022
Cited by 6 | Viewed by 2082
Abstract
ABCA1 and ABCG1 are two ABC-transporters well-recognized to promote the efflux of cholesterol to apoAI and HDL, respectively. As these two ABC-transporters are critical to cholesterol metabolism, several studies have assessed the impact of ABCA1 and ABCG1 expression on cellular cholesterol homeostasis through [...] Read more.
ABCA1 and ABCG1 are two ABC-transporters well-recognized to promote the efflux of cholesterol to apoAI and HDL, respectively. As these two ABC-transporters are critical to cholesterol metabolism, several studies have assessed the impact of ABCA1 and ABCG1 expression on cellular cholesterol homeostasis through ABC-transporter ablation or overexpressing ABCA1/ABCG1. However, for the latter, there are currently no well-established in vitro models to effectively induce long-term ABC-transporter expression in a variety of cultured cells. Therefore, we performed proof-of-principle in vitro studies to determine whether a LoxP-Stop-LoxP (LSL) system would provide Cre-inducible ABC-transporter expression. In our studies, we transfected HEK293 cells and the HEK293-derived cell line 293-Cre cells with ABCA1-LSL and ABCG1-LSL-based plasmids. Our results showed that while the ABCA1/ABCG1 protein expression was absent in the transfected HEK293 cells, the ABCA1 and ABCG1 protein expression was detected in the 293-Cre cells transfected with ABCA1-LSL and ABCG1-LSL, respectively. When we measured cholesterol efflux in transfected 293-Cre cells, we observed an enhanced apoAI-mediated cholesterol efflux in 293-Cre cells overexpressing ABCA1, and an HDL2-mediated cholesterol efflux in 293-Cre cells constitutively expressing ABCG1. We also observed an appreciable increase in HDL3-mediated cholesterol efflux in ABCA1-overexpressing 293-Cre cells, which suggests that ABCA1 is capable of effluxing cholesterol to small HDL particles. Our proof-of-concept experiments demonstrate that the LSL-system can be used to effectively regulate ABC-transporter expression in vitro, which, in turn, allows ABCA1/ABCG1-overexpression to be extensively studied at the cellular level. Full article
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