ArticleInternational journal of molecular medicine2017
Reactive oxygen species mediate angiotensin II-induced transcytosis of low-density lipoprotein across endothelial cells.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 23 citations in OpenAlex.
- Complex of Angiotensin II with Modified Low-Density Lipoproteins: Behavioral and Hemodynamic Effects in Rats.Bulletin of experimental biology and medicine · 2024Article
- Metabolite, Biochemical, and Dietary Intake Alterations Associated with Lifestyle Interventions in Obese and Overweight Malaysian Women.Nutrients · 2024Article
- Increased caveolin 1 by human antigen R exacerbatesCytoJournal · 2024Article
- Qiqilian ameliorates vascular endothelial dysfunction by inhibiting NLRP3-ASC inflammasome activationPharmaceutical biology · 2023Article
- Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells.International journal of molecular sciences · 2023Review
- The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.Immunity, inflammation and disease · 2023Review
- Single-Cell Transcriptome Analysis Reveals the Role of Pancreatic Secretome in COVID-19 Associated Multi-organ Dysfunctions.Interdisciplinary sciences, computational life sciences · 2022Article
- Atherogenesis, Transcytosis, and the Transmural Cholesterol Flux: A Critical Review.Oxidative medicine and cellular longevity · 2022Review
- Transcytosis of Galectin-3 in Mouse Intestine.Methods in molecular biology (Clifton, N.J.) · 2022Article
- A role for aldehyde dehydrogenase (ALDH) 2 in angiotensin II-mediated decrease in angiogenesis of coronary endothelial cells.Microvascular research · 2021Article
- Transport of LDLs into the arterial wall: impact in atherosclerosis.Current opinion in lipidology · 2020Review
- Low density lipoprotein mimics insulin action on autophagy and glucose uptake in endothelial cells.Scientific reports · 2019Article
- Endothelial permeability, LDL deposition, and cardiovascular risk factors-a review.Cardiovascular research · 2018 · on this mapReview
- ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).Advances in experimental medicine and biology · 2017Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retention of plasma low-density lipoprotein (LDL) particles to subendothelial spaces through transcytosis across the endothelium is the initial step of atherosclerosis (AS). Angiotensin II (Ang II), as the principal effector molecule of the renin-angiotensin system (RAS), is implicated in several important steps of AS development. However, whether or not Ang II can directly exert a pro‑atherogenic effect by promoting LDL transcytosis across endothelial barriers, has not been defined. In the present study, we found that Ang II upregulated intracellular reactive oxygen species (ROS) levels in endothelial cells (ECs) by measuring fluorescence of 2',7'-dichlorofluorescein (DCF‑DA). Based on our transcytosis model, we observed that Ang II significantly accelerated LDL transcytosis, whereas transcytosis inhibitor methyl-β-cyclodextrin (MβCD) and ROS inhibitor dithiothreitol (DTT), markedly blocked the Ang II-stimulated increase in LDL transcytosis. Confocal imaging analysis revealed that both LDL uptake by cells and LDL retention in human umbilical venous walls were highly elevated after Ang II exposure, while MβCD and DTT significantly inhibited the effects of Ang II. What is more, proteins involved in caveolae-mediated transcytosis, including LDL receptor (LDLR), caveolin-1 and cavin-1, were associated with Ang II-induced LDL transcytosis across the ECs. Nevertheless, this process was independent of clathrin in our study. Of note, ROS inhibitor, DTT, markedly decreased the expression levels of those proteins. Consequently, ROS are critical mediators in Ang II-induced LDL transcytosis. Hopefully, these findings will provide novel insight into the crosstalk between dyslipidemia and RAS in atherogenesis.
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