ABCG1 and HDL in Health and Disease

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: 2 January 2025 | Viewed by 928

Special Issue Editors


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Guest Editor
Department of Food, Nutrition, and Packaging Sciences, College of Agriculture, Forestry & Life Sciences, Clemson University, Clemson, SC 29634, USA
Interests: ABCA1; ABCG1; atherosclerosis; cholesterol efflux; miR-33; reverse cholesterol transport

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Guest Editor
Clemson Light Imaging Facility, Clemson University, Clemson, SC 29634, USA
Interests: biomarker; cell biology; exosome; extracellular vesicle; nanoparticle

Special Issue Information

Dear Colleagues,

Intracellular cholesterol content is crucial to influencing several conditions and disease states, as altering intracellular cholesterol levels impacts membrane fluidity, lipid raft formation/disruption, and signaling pathways. Cellular cholesterol metabolism is regulated by numerous factors and the removal of cellular cholesterol is considered to be primarily controlled by cholesterol efflux. Two major proteins which regulate cholesterol efflux are the transporter ABCG1 and the lipoprotein HDL. However, both of these proteins appear to modulate other biological effects besides the removal of cholesterol. For instance, ABCG1 expression has been shown to be anti-inflammatory, and HDL is considered to have both antioxidant and anti-inflammatory properties. Interestingly, while HDL is largely thought to be atheroprotective, some data suggest certain HDL particles may be harmful to health. Moreover, it is not entirely elucidated whether the biological effects that ABCG1 and HDL exhibit rely entirely on ABCG1/HDL-mediated cholesterol efflux. It is also poorly understood whether ABCG1 expression in certain cells and tissues may either promote health or be a factor in the development of certain diseases.

This Special Issue of Biology welcomes any novel and innovative research articles as well as comprehensive reviews which focus on the impact of ABCG1 and/or HDL in the context of health and disease.

Dr. Alexis Stamatikos
Dr. Terri F. Bruce
Guest Editors

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Keywords

  • atherosclerosis
  • cancer
  • cardiovascular disease
  • cholesterol efflux
  • diet-related disease
  • inflammation
  • lipid raft
  • reverse cholesterol transport

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Published Papers (1 paper)

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Research

20 pages, 3024 KiB  
Article
Exosome-Mediated Transfer of X-Motif-Tagged Anti-MiR-33a-5p Antagomirs to the Medial Cells of Transduced Rabbit Carotid Arteries
by Goren Saenz-Pipaon, Bradley K. Wacker, Lianxiang Bi, Alexis Stamatikos and David A. Dichek
Biology 2024, 13(12), 965; https://doi.org/10.3390/biology13120965 - 24 Nov 2024
Viewed by 420
Abstract
Atherosclerosis is caused by the accumulation of cholesterol within intimal smooth muscle cells (SMCs) and macrophages. However, the transporter ATP-binding cassette subfamily A, member 1 (ABCA1), can remove cholesterol from these intimal, cells reducing atherosclerosis. Antagomir-mediated inhibition of miR-33a-5p, a microRNA that represses [...] Read more.
Atherosclerosis is caused by the accumulation of cholesterol within intimal smooth muscle cells (SMCs) and macrophages. However, the transporter ATP-binding cassette subfamily A, member 1 (ABCA1), can remove cholesterol from these intimal, cells reducing atherosclerosis. Antagomir-mediated inhibition of miR-33a-5p, a microRNA that represses ABCA1 translation, promotes ABCA1-dependent cholesterol efflux and may impede atherosclerosis development. In our previous work, transducing cultured endothelial cells (ECs) with a helper-dependent adenoviral vector (HDAd) that expresses X-motif-tagged anti-miR-33a-5p enhanced antagomir packaging into EC-derived exosomes, which delivered the antagomir to cultured SMCs and macrophages. In this present study, we tested whether in vivo transduction of rabbit carotid artery endothelium can deliver an X-motif-tagged anti-miR-33a-5p to subendothelial cells. Rabbit carotid endothelial cells were transduced in vivo with an HDAd expressing anti-miR-33a-5p either with or without the X-motif (n = 11 arteries per vector). Contralateral carotids received HDAd that express scrambled oligonucleotides. Three days after transduction, the antagomir—without the X-motif—was detected in the intima but not in the media of transduced carotids (p = 0.062). The X-motif antagomir was detected in 82% of the intimal extracts (9 out of 11 carotids) and 27% of medial samples (3 out of 11 carotids, p = 0.031). However, the X-motif did not significantly enhance antagomir delivery to the media (p = 0.214 vs. non-X-motif antagomir). Expression of the antagomirs—with and without the X-motif—was sub-stoichiometric in ECs and SMCs. No antagomir-related changes in miR-33a-5p or ABCA1 expressions were detected. Despite its potential as a therapeutic strategy, our exosome-targeted gene transfer system requires further improvements to enhance antagomir expression and delivery to the subendothelial cells. Full article
(This article belongs to the Special Issue ABCG1 and HDL in Health and Disease)
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