ArticleJournal of cellular and molecular medicine2017
The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Apolipoproteins as potential communicators play an essential role in the pathogenesis and treatment of early atherosclerosis.International journal of biological sciences · 2023Review
- Association of serum apoA-I with in-stent restenosis in coronary heart disease.BMC cardiovascular disorders · 2022Article
- Stent-based delivery of AAV2 vectors encoding oxidation-resistant apoA1.Scientific reports · 2022Article
- D-4F Ameliorates Contrast Media-Induced Oxidative Injuries in Endothelial Cells via the AMPK/PKC Pathway.Frontiers in pharmacology · 2020Article
- Comparison of Mechanisms of Endothelial Cell Protections Between High-Density Lipoprotein and Apolipoprotein A-I Mimetic Peptide.Frontiers in pharmacology · 2019Article
- Commentary: The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.Frontiers in pharmacology · 2017Article
- Ascorbic acid relieves neuropathic pain and depressive behavior by reducing inflammation and activating antioxidant responses.Molecular painArticle
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12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
D-4F, an apolipoprotein A-I (apoA-I) mimetic peptide, possesses distinctly anti-atherogenic effects. However, the biological functions and mechanisms of D-4F on the hyperplasia of vascular smooth muscle cells (VSMCs) remain unclear. This study aimed to determine its roles in the proliferation and migration of VSMCs. In vitro, D-4F inhibited VSMC proliferation and migration induced by ox-LDL in a dose-dependent manner. D-4F up-regulated heme oxygenase-1 (HO-1) expression in VSMCs, and the PI3K/Akt/AMP-activated protein kinase (AMPK) pathway was involved in these processes. HO-1 down-regulation with siRNA or inhibition with zinc protoporphyrin (Znpp) impaired the protective effects of D-4F on the oxidative stress and the proliferation and migration of VSMCs. Moreover, down-regulation of ATP-binding cassette transporter A1 (ABCA1) abolished the activation of Akt and AMPK, the up-regulation of HO-1 and the anti-oxidative effects of D-4F. In vivo, D-4F restrained neointimal formation and oxidative stress of carotid arteries in balloon-injured Sprague Dawley rats. And inhibition of HO-1 with Znpp decreased the inhibitory effects of D-4F on neointimal formation and ROS production in arteries. In conclusion, D-4F inhibited VSMC proliferation and migration in vitro and neointimal formation in vivo through HO-1 up-regulation, which provided a novel prophylactic and therapeutic strategy for anti-restenosis of arteries.
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